Muted group theory: Research

Muted group theory: Research Abstract The motivation behind this report is to research the muted group theory, for the purpose to spread the finding to students taking the level 200 communications paper, this theory may be used in the final exam for this paper so there is a large necessity for the finding to be correct. While it is hard to understand the interest in this feminist theory there is an underlying interest fact for both male and female students. The problem in this report is the misunderstanding on the theory, the name itself is misleading, giving a misconception that it has something to do with the physical inability to speak. The way this problem was solved was through a collection and evaluation of various books and articles related, n some cases mildly and others majorly, to the theory. The result from the research that was done was that, in short, the muted group theory is a mental problem where through the dominant group of a culture the mute group is forced into alliteration. This theory is important; it points out the obvious ideas about female cultures and explains reasons behind what they are, how they become that way and who makes it happen. Introduction The purpose of this report is to gain the knowledge of what the mute group theory is, who researched the theory, why they did, how it contributed to the way we communication and what is the future for this theory. The intended way in which this will be achieved is through researching the theorists findings and collectively reporting on them, in a way in which my audience will understand. The limitations of this report were mainly funding, to gain access the most of the theorists articles, paid logins were required, or the funding to buy books that arent readily accessible. Another limitation was the catalogue at the Whitireia library, while there were an abundance of feminist related books there was a limited amount related to this in particular theory. The ability to read an index, I found myself looking for a replacement book in the last few days when I realised that the one I was using had nothing to do with Kramarae. Lack of knowledge, towards the end of the time I had for the report I discovered that Kramarae had a different name for a period of her research. Lastly, time management was a major limitation. The methods used to research this theory were books from the library, articles from Proquest and articles researched from the internet. In this report you will find a literature review, the findings, Conclusion, a summary of points of information and a critique of the theory. Literature Review Two Books Belenky, M. F. (1986). Womens ways of knowing: the development of self, voice and mind. In Introduction (pp.4-17). New York: Basic books. Kramarae is used in the introduction chapters as an example into the background of the study. In this section the author discussed the feelings of women not being served adequately on their needs as women, the idea that women find it harder to establish themselves in roles of authority, talking about the suggestion that women as often unheard or ignored in most situations even when they feel that they know something important that should be shared, along with the feeling of being ignored they feel they are being discouraged from practising any intellectual line of work that is typically male dominated as it is seen as being ‘unfeminine and unreachable with what women are suppose to be capable of. It is an unspoken idea amongst the male culture that women should e seen but not heard. Even now in the modern world, where things have supposably changed it is still relatively rare to find females in roles of authority. I found this book to have the third largest amount of detail on my theory from the books Whitireia library had to offer. The first being Readings in Feminist Rhetorical Theory the second being my text book. I was disappointed with the lack of direct mention of the mute group theory. I found that I had to read between the lines to gather anything helpful from this book. Not helpful, was the fact that in this small section of a chapter the author was using a multitude of examples from various theorists to explain herself. Griffen, C. L., Foss, K. A., Foss, S. K. (2004). Readings in Feminist Rhetorical Theory. In Cheris Kramarae (pp. 8-44). Thousand Oaks, Calif: Sage Publications. The chapter of this book devoted to Cheris Kramarae opens with a background of her development of education and how she became interested wit this theory. Moving on to the first section ‘Proprietors of language this section discusses the idea that in a male dominated culture the language is developed by male without consideration of females (the dominate group develops the language without consideration of the mute ­Ã‚ ­ group). The next section is titled ‘women as a way males/dominate groups inconsideration of the female/muted groups forces the compression of the muted group to begin with, i.e. having no connection to the culture dominate norms pushes the group deeper into decline. The third is ‘a visiting scholar talks about the oppression of past female scholars and their research making the present research redundant and repetitive if it had been openly accessible. The next ‘Do we really want more control of technology discusses the possible idea that technology cold release the muted group by giving them the opportunity to be a part of the new language developed with the new culture the technology is producing, also the sceptical again this idea. The final chapter titled ‘Feminist theories of communication discusses the multiple other female theories, these are all directed solely towards female culture while most non-feminist theory doesnt take this into account and results in misleading and dangerous ideas in relation to womens experiences. I found that the majority of this chapter didnt directed related to mute group theory more about feminist theories in general and relating them quietly to the mute group theory. But the points that are discussed are interesting while only slightly topical. Being only written five years ago found it did appear rather outdated when talking about technology. Two Database Articles Cheris Kramarae. (2003). Women, Work and Computing / Unlocking the Clubhouse: Women in Computing. Review of medium_being_reviewed title_of_work_reviewed_in_italics. NWSA Journal, 15(2), 207-210. Retrieved August 17, 2009, from Research Library. (Document ID: 423976331). This article is a response to an earlier article on the relationship between women and the computer industry The article points out that the percentage of women in this industry is declining but the is little know of why the original article was about Ruth Woodfield, Jane Margolis and Allan Fishers research into this mystery. They conclude with the reasoning of the culture of computing still being male dominated, there is still the potential though, for female to break through this. This article discusses the idea of genderless universe allowing a theoretical ‘reset on the idea on society in the virtual world this is plausible but in the physical it is impossible in regards to male superiors over employees, also many dominate group fear the idea of gender bending they do not want to be deceived or loss there power. This idea does not seem like it would conclude with the potential goal set foreword. Finally two points are pointed out that were missed from the initial article, there was no mention of race issues in obtaining degrees and secondly that the females that do pervade in this industry are stereotyped hostility with underserved labels. I found this article less than helpful in comparison to the other reading I collected, while it was written by the theorist herself there was little to no mention directly on the mute group theory, which I expected from the title. Although there are many points that I myself would relate easily to her theory. Cheris Kramarae. (2005). Muted Group Theory1 and Communication: Asking Dangerous Questions. Review of medium_being_reviewed title_of_work_reviewed_in_italics. Women and Language, 28(2), 55-61,72. Retrieved August 17, 2009, from Research Library. (Document ID: 974623021) Kramarae explains examples about mute group theories mainly on the constraints of women due to the donate male group ‘belittling their intellectual property, and academic works, she explains about how language is male oriented and is subjective against women. She also talks about the relation of other cultures and races with the mute group theory. She then movies on to the history of muted women for the past 500 years and how when she first started working on her theory it was radical and topical, people were interested and fascinated but now this not so interesting, she puts this up to the fact that the world must be changing and fixing itself through technology, changing the definitions of the original male defined language with less discomfort in the words that are used commonly in society. After that she compares standpoint theory with mute group theories, both theories relate the different in gender perception to their differing experiences and affects of their views. Empathy towards others and trying to see others views could help solve many group problems. Mute group theories looks at groups while standpoint looks at the individual. Later she points out that by trying to use the group theory; results can easily turn into essentialism by trying to not miss a viewpoint of a group you can look over another. This article was written by Cheris Kramarae herself, talking directly about her very own theory, by my option I would say that makes the article very accurate. It was a Journal from Proquest. Two Internet Articles Baer, J. (2009). Muted Group Theory by Cheris Kramarae. Retrieved August 18, 2009, from University of Colorado at Boulder web site: http://www.colorado.edu/Communication/meta-discourses/Papers/App_Papers/Baer.htm This paper refers to both theorists Kramarae and Ardener (female and male), and describes there different approaches. Ardener seeing women as being constructed differently causing differences in the way they act. Defining muteness as being lower in status than the dominate group. Kramarae differs, defining muteness as the lack of power a group holds. She says that women a perceived as not only holds. She says that women a perceived as not only being less powerful, but also as a group use a different language than the dominant group. This language to men is harder to understand as it is not worth it. Muteness is a dominant-group created problem. The next section is a case study explaining a work situation where there are two males and four females. Where the two males and one of the females are higher positions and the other three females are there assistants. The female that is in a higher role is there through conversion to the male manners to gain their acceptances, by relation her assistant was also accepted by the males and they listened to both. The other two female assistants were treated as lesser valued workers, while they acted like females they were treated as well by their overheads, but their ideas in relation to the work were ignored or suppressed to gain the clients respect. The last section is the critique of the theory. The writer of this paper tends to agree with the proposed ideas with the muted group theory. Making points on her own evidence that for the 25 years Kramarae worked on muted group theory there was little change and nothing very big. Not much change in the way women are viewed between 1970s and 1990s. This paper was very relevant to the mute group theory, it compared the two theorists and gave a real life example, although it would have been more interesting if it was written by a male instead of another female. McLaughlin, D. (1999). Research report on Edwin Ardeners â€Å"Belief and the Problem of Women†. Retrieved August 18, 2009, from Oak University Website http://oak.cats.ohiou.edu/~dm419397/mgres.htm This is a report on the Edwin Ardeners article ‘Belief and the problem with women. The author D.McLaughlin reports on this simular theorist to get a further view of the theory. Ardener and Kramarae share the same ideas of the theory, that women or the muted group are muted by the unfairness in their language from the male or dominate group. The differences found in the theorist are that Ardener splits his theory in two parts, technical and analytical. Technical, in which the point of man-made language falls, women that cannot communicate through this dialect are outcast as inarticulate. Analytical, in which women have to work harder in society to provable and must change to fit the male norms. This was researched through the observation of the Cameroon tribes, where females would have to participate in ‘rite s of passage rituals including seclusion, tests and rapes. Once past, they would be rewarded with respect and acceptance from the males. Ardeners; idea of women is that their ultimate goal is to achieve the respect of male to be on a ‘level playing field. The author concludes with the idea that this comparison is a symbolic look at our male dominated society in regards to the Cameroon tribes, that women everywhere must adjust their ways to achieve male acceptance. I found it interesting to read the male theorists take on the mute group theory, although I was disappointed by the fact that there definitions were incredibility simular, I did find that his comparison of the western culture and Cameroon tribes helped me understand the ideas that arise though his take on the theory. While the article was on a male theorist it was written by a female student, I would be more interested to get a purely male take on the theory. Findings Background Of Theorist Cheris Kramarae was born 1938 in South Dakota. Throughout the sixties and seventies she gain a B.S. degree in journalism and English, an M.S. degree in journalism and English and a Ph.D. in speech Communication, she then went on to teach in the speech Communication department at the University of Illinois. She then focused her work in the structure and use of language. Outline Of The Theory/key Issues To define muted group theory, the muted group must first be defined. The muted group are not technically mute, but though the language their culture supplies them with, are unable to articulate themselves to the extent of the non-muted or dominate group, the dominate group being the superior group of people in the culture that hold the power to the decisions that define the culture, they take little to no consideration to the non-dominant or muted groups in their culture when creating the norms, through which pushing the muted group further into recession. The muted group theory is the theory through which this group occurs, with the dominate groups invention of the language without the thought of the recessed group. The mute group differs from the dominant though their experiences and perceptions of these. Kramaraes theory is mainly feminist oriented, the mute group being woman and the dominant being men. Women are seen in society as lower beings compared to men, seldom involved in promotions in the workplace when there is another alternative along with examples like being tricked into being kept ‘in their place. Application Of The Theory With the rate technology is advancing Karamaraes vision for the next steep of her theory is the movement into online communication interaction. Her idea is that online a person can be genderless, making communication uncontrolled by the muted group theory to abolish the norm of sexes getting different treatment according to their significance in society. To be treated other than mindless helpers to the dominant group, men, women must change the way they are perceived by men to be accepted by men, when they are accepted they then gain the respect of men and are treated like they belong to the dominant group, the way this is done is that a woman must adopt the characteristics of a male, using their language the way it was intended by the dominant group and copying there mannerisms. With the advances through technology, the internet has provided us with the environment and means, though with Kramaraes vision of the need to lose the female mannerisms to be accepted. With the new networki ng tools web 2.0 provided us with we can know create a new unbiased driven characters with sites like second life and games like world of Facebook. The dominant group however despise this idea, they are terrified at the idea that the power could shift, even the smallest degree so that muted groups proposals could be seen as important, or even more important than the current dominant group, hating the idea of even the possibility that Kramarae could be right they would never accept that women have their own personal language, to the dominant group all they are concerned with is power and how to use it against people. Evaluation Of The Theory Kramarae believes that women are the westerns cultures muted group of our culture, they are the repressed group driven into illiteracy through the actions of the dominate male group of our culture, creating the language we are forced to use daily through the raw fact that there is now alternative means to communication. To be accepted and pull themselves out from the depths of the male created recession, they must gain the respect of males through copying them and gaining acceptance into their dominant group. Kramarae hopes that this could be over come through the use of technology, changing our culture from dominant and muted groups to one large genderless group. Conclusion The reason this theory is important in society is it raises issues about the female culture, how they are formed through their experiences, and since their experiences differ from males they shape differing norms then males and since males norms are society norms, females not fit in. Do you find yourself questioning the way youre seen in the world? Are you naturally part of the dominant culture that will end up in a highly respected job role? Or are you part of the muted group being ignored while others are getting the recognition that you deserve? Or you in the dominant group, after gaining the respect from you new pears by throwing away the traits of your natural muted group? Will the future bring the genderless society that Kramarae wants? Its hard to tell, but from the little mention of this theory since the 90s it seems that perhaps its already happening. A Summary Of Points Of Information Kramarae focused her work in the structure and use of language. The mute group are the non-dominant people in a culture, unable to articulate themselves to the extent of the dominant group. In western culture this is the female group. Dominant group are the power holders of the culture, making the decisions that define the culture. In the western culture this is the male group The dominant group defines the culture to their norms. The groups differ mainly upon experiences and how their perceptions are formed through these. Kramaraes theory can be applied to online communication interaction Online a person can be genderless Genderless meaning that the rules and norms of their group are abolished. To be accepted by the dominant group, members of the muted group adopt the ways of that group. The ways of the dominant group being the way they use the language and their mannerisms. The genderless communication is can be applied through networking sites that are now readily accessible to anyone, for example Facebook or second life. The dominant group are concerned with this idea and find objectionable the idea of losing the power that they currently can use against people. A Critique Of The Theory When I began my research of this theory I thought that it was totally different from what it actually was. I had no idea that I was expected to research a feminist theory of with I am morally against. But once I studied Kramaraes findings I found myself confused about my opinion upon the theory. I got angry at the idea of this theory, I am not a stereotypical female in theory, and I participate in many male typical hobbies and in general am a bit of a ‘tom boy. So when I read Kramaraes generalisations about the female culture it annoyed me that I was supposed to fit into this generalisation. I found myself ranting at people about how this theory was so close minded and did not take into account the people who do not fit into these categorises. Once I had finished researching my topic I was still annoyed but from a different position, I was now able to agree with the theory on many levels, it makes sense. The idea was females being put lower in importance in this culture and the males being the decision makings, its true as all the years ago when these norms were established women we discouraged entirely from pursuing any type of power oriented positions. Now days its changed, women can gain these powerful positions and that all fits into Kramaraes theory, to get to these positions women must change their ways to gain the respect from the dominant group, adopting the characteristics of the males. I dont want to accept it but I guess that my ‘tom boy mannerisms can fit into this as trying to gain the respect of the males that I associate myself with. This theory was discovered by a female, most of the articles I read on the theory were written by females, the article I read on male viewpoint on the theory was written by a female. I think it would have been much more interesting to have more male inputs into this theory. It is my opinion that a male student should have been assigned this theory to research. Glossary Of Terms Dominant: the state that exists when one person or group has power over another; her apparent dominance of her husband was really her attempt to make him pay attention to her Mute/ muted: the equaliser of the dominant group, with a dominant group there is always the muted group. When one person or group has power over another, the power is taken away from the muted group to retain balance. Group: any number of entities (members) considered as a unit Theory: A hypothesis that has withstood extensive testing by a variety of methods, and in which a higher degree of certainty may be placed. A theory is NEVER a fact, but instead is an attempt to explain one or more facts Culture: the attitudes and behaviour that are characteristic of a particular social group or organization Genderless: Without an associated gender Facebook: Facebook is a free-access social networking website that is operated and privately owned by Facebook, Inc Second life: is an online 3D interactive virtual reality program which resembles console video games such as Final Fantasy, but is almost entirely built and influenced by the people who use it References Belenky, M. F. (1986). Womens ways of knowing: the development of self, voice and mind. In Introduction (pp.4-17). New York: Basic books. Griffen, C. L., Foss, K. A., Foss, S. K. (2004). Readings in Feminist Rhetorical Theory. In Cheris Kramarae (pp. 8-44). Thousand Oaks, Calif: Sage Publications. Cheris Kramarae. (2003). Women, Work and Computing / Unlocking the Clubhouse: Women in Computing. Review of medium_being_reviewed title_of_work_reviewed_in_italics. NWSA Journal, 15(2), 207-210. Retrieved August 17, 2009, from Research Library. (Document ID: 423976331). Cheris Kramarae. (2005). Muted Group Theory1 and Communication: Asking Dangerous Questions. Review of medium_being_reviewed title_of_work_reviewed_in_italics. Women and Language, 28(2), 55-61,72. Retrieved August 17, 2009, from Research Library. (Document ID: 974623021) Baer, J. (2009). Muted Group Theory by Cheris Kramarae. Retrieved August 18, 2009, from University of Colorado at Boulder web site: http://www.colorado.edu/Communication/meta-discourses/Papers/App_Papers/Baer.htm McLaughlin, D. (1999). Research report on Edwin Ardeners â€Å"Belief and the Problem of Women†. Retrieved August 18, 2009, from Oak University Website http://oak.cats.ohiou.edu/~dm419397/mgres.htm Griffin, E. (2009). A first look at communication theory (7th ed.). In Muted group theory of Cheris Kramarae (pp. 454-465). New York: McGraw Hill. Bibliography CMM. (2009). Retrieved August 19, 2009, from http://oregonstate.edu/instruct/theory/mutedgrp.html Cari Porter. (1999). Muted Group Theory. Retrieved August 4, 2009, from http://oak.cats.ohiou.edu/~cp300795/mg.htm Wikipedia. (2009). Muted group theory Wikipedia, the free encyclopedia. Retrieved August 19, 2009, from http://en.wikipedia.org/wiki/Muted_group_theory WordNet Search 3.0. (2009). Retrieved September 11, 2009, from http://wordnetweb.princeton.edu/perl/webwn?s=dominance WordNet Search 3.0. (2009). Retrieved September 11, 2009, from http://wordnetweb.princeton.edu/perl/webwn?s=group WordNet Search 3.0. (2009). Retrieved September 11, 2009, from http://wordnetweb.princeton.edu/perl/webwn?s=culture Define: second life Google Search. (2009). Retrieved September 2009, from http://www.google.co.nz/search?hl=enclient=firefox-arls=org.mozilla%3Aen-US%3Aofficialq=define%3A+second+lifebtnG=Searchmeta= TERMS AND DEFINITIONS FOR QUIZ.(2004).Retrieved September 11, 2009, from http://blue.utb.edu/biology/oliva/terms_and_definitions_for_quiz_1.htm Facebook Wikipedia, the free encyclopedia. (2009). Retrieved September 11, 2009, from http://en.wikipedia.org/wiki/Facebook Genderless – Wiktionary (2009). Retrieved September 11, 2009, from http://en.wiktionary.org/wiki/genderless 20800537 2 / 15 Gestational diabetes: An analysis Gestational diabetes: An analysis Gestational diabetes: consequences for fetal programming of vascular disease in adulthood List of Abbreviations AGE Advanced Glycation End Products CNS- Central Nervous System EDHF- Endothelium-Derived Hyperpolarising Factor eNOS Endothelium derived Nitric Oxide ECM- Extra Cellular Matrix FFA Free Fatty Acids GAD 65- Glutamic Acid Decarboxylase GDM-Gestational Diabetes Mellitus HDL- High Density Lipoprotein HPL- Human Placental Lactogen IA-2 Insulinoma- Associated Antigen 2 ICA- Islet Cell Antibody IRS-1 Insulin Receptor Substrate 1 IUGR Intrauterine Growth Restriction LDL- Low Density Lipoprotein MODY- Maturity Onset Disease of the Young MRS- Magnetic Resonance Spectroscopy NO Nitric Oxide OS- Oxidative Stress PKC- Protein Kinase C ROS Reactive Oxygen species TNF-ÃŽ ±- Tumour Necrosis Factor ÃŽ ± T1D Type 1 Diabetes T2D Type 2 Diabetes ZnT8 Zinc Transporter 5-HT Serotonin Abstract Gestational Diabetes is a condition present in the later stages of pregnancy where the mother has insulin resistance leading to glucose intolerance. The aetiology of Gestational Diabetes Mellitus is largely unknown but several theories include autoimmune destruction of the beta cells, monogenic mutations and insulin resistance. In pregnancy it is normal for there to be some levels of insulin resistance and it is thought that the products of the placenta contribute to the state of insulin resistance as GDM usually subsides after pregnancy. GDM in pregnancy can lead to an increased risk of cardiovascular disease in the offspring such as hypertension and atherosclerosis. This is due to the increased levels of oxidative stress and inflammatory mediators present during pregnancy. The placenta is very important as it is able to control and buffer the amount of glucose that is delivered to the fetus but if this level is too high then it is out of the placentas control and the fetus may have increased rate of growth due to this extra glucose. The current focus of research in this area seems to be into finding ways to diagnosis GDM earlier in the pregnancy and to try and reduce the amounts of oxidative stress. Gestational diabetes: consequences for fetal programming of vascular disease in adulthood Introduction Gestational Diabetes Mellitus (GDM) occurs when there is a glucose intolerance that is first detected during pregnancy. It is a form of hyperglycaemia (Buchanan and Xiang 2005). The aetiology of the condition is unknown but there have been many suggestions as to the cause of it, including autoimmune destruction of the ÃŽ ² pancreatic cells and the possibility of a genetic predisposition to the condition. Hormones that are produced in pregnancy help contribute to the insulin resistant state which characterises diabetes. In recent years, there has been an increase in the cases of Obesity and this is a risk factor for both Diabetes Mellitus and Cardiovascular Disease. The intrauterine environment can affect fetal programming and development. This essay will look into how the placenta and its products can affect the insulin resistant state and how this resistance effects programming as well as the role of oxidative stress and inflammation in making the offspring more susceptible to cardi ovascular disease. Gestational Diabetes Mellitus (GDM) GDM is a state of insulin resistance which disturbs the intrauterine environment and can lead to accelerated fetal growth (Radaelli et al 2003).It effects approximately 7% of pregnant women with approximately 200,000 cases seen each year (Schillan-Koliopoulos and Guadagno 2006). The term GDM is applicable when the onset is during the second and third terms of the pregnancy, but it does not exclude the possibility that the insulin resistance was undiagnosed before the pregnancy. If this is the case and is found to occur in the earlier stages of pregnancy then the mother should be treated the same as mothers who are known to have diabetes before pregnancy (Metzger, Coustan 1998). There is a degree of insulin resistance in normal pregnancy which begins towards the middle of the pregnancy but during the later part of the second and the final trimester these can increase to levels of insulin resistance that are associated with type 2 diabetes (Yogev et al 2008 Chapter 10). Insulin resistance is when the tissues do not produce a response to insulin due to problems with the secretion of insulin or where the tissues are desensitised to insulin and therefore lack the ability to produce a response (Catalano et al 2003). In a normal pregnancy, the mother changes her metabolism to allow a constant supply of nutrients to reach the fetus to support its rapid growth. Among these nutrients is glucose, which is the main energy source used by the fetus. During the later stages of pregnancy the mother becomes hypoglycaemic and although there is increased gluconeogenesis, the hypoglycaemia still occurs because there is a high rate of transport of glucose to the fetus (Herrera 2000 cited in Herrera and Ortega 2008). GDM can have effects that impact the development of the fetus such as hypoglycaemia and macrosomia, which is an increase in body weight and has the possibility of leading to problems when giving birth, such as shoulder dystocia (Schillan-Koliopoulos and Guadagno 2006). During the second trimester of pregnancy there is peripheral insulin resistance but there is also the possibility that hepatic insulin sensitivity is altered in pregnancy, although few studies confirm this. By the end of the pregnanc y the levels of insulin that are circulating are thought to be double those at the start (Redman 2001). Insulin Resistance Insulin resistance in GDM can occur in two forms. The first is where it develops in late pregnancy and it has been postulated that there is a post-receptor mechanism that may influence the insulin signalling pathway which leads to a reduced glucose uptake. The second form is where there is already a degree of resistance before the pregnancy but the changes that occur in normal pregnancy aggravate this (Metznger et al 2007). The insulin resistance that develops in pregnancy is much needed to allow the flow of nutrients, from the mother, directly to the fetus to allow for growth (Radaelli 2003). Increased insulin resistance leads to an increase in insulin secretion by the ÃŽ ² pancreatic cells (Buchanan and Xiang 2005). The insulin resistance is thought to be caused by increased adiposity and as the insulin resistance usually stops after pregnancy this suggests that there is a possibility that the products of the placenta are a potential cause of the resistance. During the course of the pregnancy the actual changes in glucose levels are very small. It would be assumed that the glucose levels would rise due to the increased insulin resistance but the pancreatic ÃŽ ² cells increase their secretion of insulin to maintain homeostatic glucose levels (Yogev et al 2008 Chapter 10). GDM occurs because there is an increased demand for insulin which under normal circumstances can be met unless there are problems with the secretion of insulin leading to the development of hyperglycaemia. The majority of mothers who develop GDM have been discovered to have a degree of insulin resistance before they became pregnant. Therefore, with the insulin resistance that occurs in normal pregnancy it can be said that GDM occurs with a greater insulin resistance than normally present in gestation (Yogev et al 2008 Chapter 10). Insulin resistance causes a decreased uptake of glucose into skeletal muscle, adipose tissue and liver as well as a decreased production of hepatic glucose. (Catalano et al 2003). One suggestion for insulin resistance looks into the possible role of the mitochondria. Studies using Magnetic Resonance Spectroscopy (MRS) have shown that in normal offspring of parents with type 2 diabetes, there is an increased amount of intramyocellular lipid. This has been shown to cause a reduced function in mitochondria which suggests that mitochondrial dysfunction may play a part in insulin resistance (Petersen et al 2004 cited in Morino et al 2005). It has been suggested that this increase in intramyocellular lipid activates a serine kinase cascade which causes an increase in the Insulin Substrate Receptor 1 (IRS-1), which inhibits insulin receptor phosphorylation on tyrosine sites. This can cause a decrease in the effects and utilisation of glucose. One study showed that in the insulin resistant offspring the mitochondrial density was reduced by just over a third to that of a normal offspring. This suggests that offspring who are insulin resistant may inherit a condition th at causes a reduction in rate oxidative phosphorylation in mitochondria (Griffin et al 2009 cited in Morino et al 2005). Detection of GDM Diagnosis of GDM helps to identify pregnancies that are at risk of fetal morbidity as well as obesity and glucose intolerance in the offspring (Buchanan and Xiang 2005). GDM is hard to diagnose as it is asymptomatic. Normal diabetes could be diagnosed by glycosuria but in pregnancy the renal threshold to glucose is lowered so that glycosuria doesnt give a true representation of hyperglycaemia (Redman 2001). There are several risk factors of GDM which can be classified into three groups and help in the screening process. Low risk factors include women who are younger than 25, normal weight at conception, no known family members with diabetes and no history of glucose intolerance. High risk factors include obesity of the mother, diabetes in close relatives, a history of glucose intolerance, current glycosuria and previous pregnancies with GDM (Metzger and Coustan 1998 Chapter 25). Causes of Diabetes There are several theories as to why diabetes occurs and this has been thought to be similar to the underlying mechanisms that cause gestational diabetes. Diabetes is a result of pancreatic beta-cell dysfunction which can present in three main ways: autoimmune, a genetic cause and on top of already present insulin resistance (Buchanan and Xiang 2005). Autoimmune diabetes accounts for approximately 5-10% of all diabetic cases (American Diabetes Association 2010). There are circulating antibodies to the ÃŽ ² cells of the Islet of Langerhans. In GDM, there are a small number of women who have with these antibodies present in their circulation. It is thought that these cases present with GDM due to problems with insulin secretion caused by destruction of the Islets by the autoantibodies (Buchanan and Xiang 2005). This form is similar to type 1 diabetes. The Islet Cell Autoantibodies (ICA) have been shown to have four major molecular targets: Insulin, Glutamic acid decarboxylase (GAD 65), Insulinoma-associated antigen-2 (IA-2) and Zinc Transporter 8 (ZnT8) (Tree 2010). Monogenic diabetes has 2 general forms, one where there are mutations in autosomes and the other where there are mutations in the DNA of mitochondria. The first form is commonly referred to as Maturity Onset Diabetes of the Young (MODY). In both cases onset tends to be at a young age and the patient doesnt present with insulin resistance or obesity (Buchanan and Xiang 2005). Mutations that cause MODY have been found in some women with GDM and commonly occur in genes coding for glucokinase, hepatocyte nuclear factor and insulin promoter factor, MODY is associated with beta cell dysfunction (Weng et al 2002). Chronic insulin resistance with beta-cell dysfunction seems to be the most common cause of GDM. As mentioned before there is an increase in insulin resistance in normal pregnancy but if this develops with background insulin resistance then there is an even greater insulin resistance which can lead to GDM. An established suggestion is that women who are unable to increase their secretion of insulin to cope with the insulin resistance developed in late pregnancy are more susceptible to developing GDM (Buchanan and Xiang 2005). However there could be various environmental processes that are involved in the underlying pathophysiology of GDM. The products of the placenta may also have a role in increasing or decreasing insulin resistance and these will be discussed later. Placental Function The placenta is an organ that has many roles during the development of the fetus. One of these functions is that it acts as a barrier to separate the maternal and fetal surfaces such that the syncytiotrophoblast surface exposes the placenta to the maternal circulation and the endothelium is exposed to the fetal circulation. This position between the two circulations means that the placenta is influenced by molecules from both circulatory systems, including cytokines, hormones and growth factors. The placenta produces molecules which can separately affect the maternal and fetal circulation and it expresses a large number of cytokines including leptin, resistin and tumour necrosis factor. However it has been discovered that these molecules are also produced by adipocytes. All molecules that are going from the mother to the fetus have to cross the placenta. Here they are either modified, for example lipids or like glucose, they are metabolised for placental purposes (Desoye et al 2008). The placenta plays an important role in fetal growth and the regulation of pregnancy (Giachini 2008). The placenta acts to sustain normal homeostatic levels and to carry out the functions of the vital organs. It also provides an immunological defence to the fetus and allows the exchange of molecules vital to its development (Jansson and Taylor 2007). Placental Development Approximately 4-5 days after conception, the process of cleavage causes rapid cell divisions and one of the groups of cells to form are called trophoblast cells. Further developmental processes form the blastocyte which is surrounded by an outer layer of the trophoblast cells. As the pregnancy progresses, the trophoblast cells develop into the placenta while the inner parts of the blastocyte form the embryo and umbilical cord (Huppertz 2008). The blastocyte implants itself onto the epithelium of the uterus where it differentiates into a syncitiotrophoblast which is able to implant itself in the epithelium leading to it being embedded into the decidual part of the uterus (Huppertz 2008). After the attachment of the blastocyte, the trophoblast layer divides very quickly and changes into 2 layers; the inner cytotrophoblastic layer and the outer syncytiotrophoblastic mass (Gude et al 2004).The whole implantation process takes 12 days to complete and after this the fetus is fully embedded into the endometrial layer (Huppertz 2008). The chorionic plate is the surface of the placenta that faces the fetus and this is where the umbilical cord inserts. The basal plate is the surface that faces the mother which contains many types of cells including immune cells such as macrophages and killer cells to carry out the placentas immunological function. The maternal basal plate and the fetal chorionic plate converge to form the smooth chorion which is composed of three layers (Huppertz 2008). When the trophopblast invades the endothelium there is a remodelling of the uterine spinal arteries which is necessary to ensure that the fetus and the placenta receive an adequate blood and nutrient supply and is able to remove any waste materials. This direct supply of blood and nutrients to the placenta can define it as being haemochorial villous organ (Gude et al 2004). After the rapid divisions of the trophoblast and development into 2 layers there are two pathways that can occur, the villous and extravillious pathways. The extravillious pathway results in the trophoblast being able to invade into the decidua and cause the remodelling of the uterine arteries to increase blood supply to the placento-fetal unit. The villious pathway has a transportation function as well as having endocrine and protective functions (Gude et al 2004). Normal Placentation Placentation involves the structure and function of the placenta. The process of placentation is helped by the composition and arrangement of the extracellular matrix (ECM) of the endometrium. Studies on rats induced with diabetes provided results that showed that diabetes has an effect on the distribution of the ECM molecules. This study by Giachini et al illustrates that Types I and III collagen as well as other molecules, such as proteoglycan molecules decorin and biglycan were distributed throughout normal and diabetic placentas. It was shown that diabetes affects the expression of fibronectin and an increase in deposition of fibronectin may cause changes to the ECM structure which could affect the transfer of molecules from the mother to the fetus. One way in which changes in the ECM can be overcome is to test blood glucose levels frequently during the pregnancy and if kept in normal ranges this can dramatically decrease the prevalence of diseases and disorders present in the fe tus (Giachini et al 2008). As the pregnancy progresses the size of the placenta increases which also means an increase in the amount of products that the placenta produces therefore increasing in the insulin resistance (Schillan-Koliopoulos and Guadagno 2006). This is because the net effect of the products of the placenta is to increase insulin resistance. The increase in size of the placenta means that it needs an increased blood supply. Failure of the mother to increase its blood supply to the placenta can lead to placental insuffiency which if exacerbated can be attributed to be a cause of intrauterine growth restriction (IUGR). This growth restriction is more related to poor maternal nutrition rather than to a cause of GDM. GDM have been associated with an increased fetal and placental weight (Jansson and Taylor 2007). One of the reasons why GDM and increased insulin resistance affects the fetus is that while glucose can cross the placenta, insulin is unable to. This means that the fetal pancreas has to compensate by producing more insulin to prevent high blood glucose levels. The fetal pancreas is capable of doing this and the liver responds to the higher levels of insulin by increasing its production of glucose (Schillan-Koliopoulos and Guadagno 2006). Offspring who have an increase in birth weight have been shown to be at risk of developing cardiovascular disease and diabetes later in life. The main risk factor for this is poor transfer of nutrients via the placenta (Jansson and Taylor 2007). How dramatic these changes are depends on how good the control of blood glucose levels have been during the development of the placenta, if any treatment has been received and if there were any periods of away from normal glucose levels (Desoye 2006). How does diabetes affect Placentation? Diabetic insults at the beginning of the pregnancy can have long last effects of the placenta. One of the roles of the placenta is that it is able to buffer excess maternal glucose which can help to keep the fetal glucose levels within range However if the insult lasts longer than the placenta is able to compensate for then excessive fetal growth may occur (Desoye Mouzon 2007). In diabetes there is endothelial dysfunction which can lead to vascular disease. The endothelial cells help to control the vascular tone of the smooth muscle lining the vasculature. They do this by producing substances that help to vasodilate the smooth muscle including Nitric Oxide, Prostacyclin and Endothelium-Derived Hyperpolarising Factor (EDHF). There have been several studies to suggest different mechanisms of how diabetes affects the endothelium including impaired release of these vasodilating molecules, faults with signal transduction and increased release of constricting mediators of the endothelium. The dysfunction of the endothelium in diabetes is thought to be caused by activation of protein kinase C (PKC) as well as increased oxidative stress, non-enzymatic glycation and an increased activation of the polyol pathway (De Vries et al 2000).The main reason why these effects occur is thought to be due the activation of the protein kinase C pathway and the increased oxidative stress. This can cause early damage to the development of vascular vessels (Roberts and Raspollini 2008). These mechanisms will be discussed later. The effect of hormones produced in pregnancy Pregnancy causes changes in the circulating hormones and cytokines which can all have different effects on insulin resistance and this may help explain the mechanism underlying the resistance that is found in pregnancy and in GDM. Cytokines produced in pregnancy, such as TNF-ÃŽ ±, Adiponectin and Leptin have been found to cause an increase in the insulin resistance (Gao et al 2008). In early pregnancy, the levels of oestrogen and progesterone rise but no net effect is seen as the two have antagonistic effects. Oestrogen increases the binding of insulin to its receptor whereas progesterone reduces the ability of insulin to bind (Ryan and Enns 1988). Cortisol levels in pregnancy increase so that by the end of the pregnancy the levels are three times that of what they were at the beginning (Gibson and Tulchinski 1980 cited in Yogev et al Chapter 10). Studies have shown that with increased amounts of cortisol there was a decrease in insulin sensitivity causing insulin resistance (Rizza et al 1982 cited in Yogev et al 2008 chapter 10). During pregnancy the levels of prolactin increase up to ten times the normal amount (Yogev et al 2008 chapter 10). Studies have shown that in a culture of pancreatic beta cells, prolactin can cause an increase in levels of secreted insulin (Sorenson et al 1993 cited in Yogev et al 2008 Chapter 10). However, high levels of prolactin are not seen to be a pathological cause of GDM (Yogev et al 2008 chapter 10). Human placental lactogen (HPL) is a hormone, and its levels rise during the second trimester of pregnancy. This causes a decrease in the phosphorylation of insulin receptor substrate (IRS1) which can lead to significant insulin resistance (Ryan and Enns 2008 cited Yogev et al 2008 ch 10). Leptin is associated with obesity and concentrations of leptin have been shown to be related to the concentration of insulin in the plasma. In pregnancy the leptin levels increase dramatically. During pregnancy the mother uses her fat stores to support fetal growth and it is thought that the leptin levels increase with the mobilisation of these fat stores. Leptin levels relate to the body mass of the individual (Sattar et al 1998). Placental Leptin is the same in structure and charge to the one produced by adipose tissue (Ashworth et al 2000). One study showed that high leptin concentrations in the umbilical cord increased the likelihood of developing fetal macrosomia (Wiznitzer et al 2000). It is also thought that leptin effects insulin sensitivity by effecting glucose metabolism in both skeletal muscle and in hepatocytes. Rats that received an external source of leptin were found to have an increase in gluconeogenesis which accounted for the majority of hepatic glucose production ( Rossetti et al 1997). In GDM there is a greater secretion of TNF-alpha in response to glucose. TNF-alpha functions to regulate metabolism of glucose and lipids as well as being involved in insulin resistance. Many studies suggest that TNF-alpha is involved in the progression to GDM. They found that an increase in glucose cause the placenta and adipose tissue to increase production of TNF-alpha in some cases up to 4 times more than non-diabetic pregnant(Coughlan et al 2001). One study showed that the increases in the levels of TNF-alpha during pregnancy increased consistently with increases in body weight (Catalano et al cited in Yogev et al 2008). Adiponectin is a protein derived from adipose tissue and its function is to regulate insulin resistance and maintains levels of glucose. During pregnancy it has been found that its levels drop and could therefore lead to the increase insulin resistance found in GDM (Gao, Yang, Zao 2008). Adiponectin has also been found to decrease the secretion of TNF-alpha which as stated above can lead to insulin resistance (Hotamisligil 1999 cited in Yogev et al Chapter 10 2008). Adiponectin may cause increased insulin sensitivity as its concentration decreases throughout the gestational period (Desoye and Mouzon 2007). Resistin is a protein that is produced by adipose tissue and is thought to be involved in insulin resistance in diabetes and is associated with obesity (Steppan and Lazar 2002) In pregnancy, resistin is secreted by the placenta and this secretion reaches its peak by the last trimester (Yura et al cited in Megia et al 2008). Studies show that TNF-alpha is an important factor in insulin resistance during pregnancy and with inputs from leptin and cortisol there is altered glucose metabolism whereas inputs from oestrogen, progesterone and prolactin had little significant effects (Kirwan and Mouzon 2002). There are many hormones produced during pregnancy, mainly by the placenta and adipose tissue that have varying affects but with the overall impact being insulin resistance. Inflammation in Diabetes There are genes in the placenta which regulate reorganisation of the endothelium and inflammatory responses and in GDM these were found to be altered. The increase in leptin receptors suggests that in the placenta this can cause proinflammatory responses (Radaelli 2003). One of the current theories is that the abnormal metabolic environment in GDM can lead to increased production of cytokines and inflammatory mediators. Molecules such as TNF-alpha, Resistin and Leptin increase during pregnancy and these increases in these inflammatory mediators produce metabolic changes by increasing insulin resistance (Desoye and Mouzon 2007). Leptin and TNF-alpha activate phospholipase A2 which are a family of eicosanoid precursors that go on to produce essential fatty acids such as w3 polyunsaturated fatty acids (Desoye Mouzon 2007). There has been a recent investigation which found that with increased adiposity at birth there has been an increase in w3 fatty acids in the placenta (Verastehpour et al 2005 cited Desoye and Mouzon 2007). As stated before, the placenta produces cytokines but it is also a site of action of the cytokines. It is the location of the receptors for these cytokines will influence if the cytokines act on the mother, the placenta or the fetus. With cytokines there is very little transfer across the placenta from mother to fetus and the origin of the cytokines in the fetus can be from either the placenta or from the fetus itself (Desoye and Mouzon 2007). Fetal Programming Many studies have highlighted the fact that events that occur while the fetus is developing can alter its developmental pathway and have adverse outcomes in later life. Fetal programming describes how the environment can affect certain developmental events of which the effects are permanent and can affect processes such as metabolism and the organisms physiology. Women with GDM have an increased risk of the fetus developing macrosomia (Catalano 2008 Chapter 11). The main factor that effects the growth of the fetus is the maternal environment and there is a strong association with the weight and height of the mother and the growth of the fetus such that mothers who are heavier and taller will produce heavy babies. (Love and Kinch 1965 cited in Catalano 2008 Chapter 11). The placenta and fetal programming The placenta is very important to the developmental processes of the fetus as it is able to change the quantity of signals and nutrients that the fetus receives. Deviation from normal would alter the fetal programming, thus making it more susceptible to disease in later life. Pregnancies that are complicated by GDM have excessive oxidative and nitrate stress which has been found to change the activity of certain proteins. Oxidative and nitrate stress alter the placentas function and may cause changes in the fetal programming. Nutrient transfer depends largely on the normal development of the vasculature to allow blood flow and this can be affected by GDM which can cause a decrease in the flow of substrates and is a mechanism in which fetal programming can be affected (Myatt 2006). Fetal programming involves a large amount of development plasticity and interruptions to this development may cause abnormalities in the development of certain cells which may progress to structural differences in organ development (Gluckman and Hanson 2004 cited in Jansson and Powell 2008 ref 16). Effects to the fetus exposed to GDM If a fetus is exposed to a diabetic environment during pregnancy then there can be certain long term effects. These effects can be classified into three groups; Anthropometric, Metabolic or Vascular and Neurological or Psychological. Anthropometric changes are concerned with the rates of growth for both height and weight and in a diabetic environment these can be excessive leading to macrosomia and obesity in later life. Metabolic and vascular changes that occur are abnormal glucose tolerance which can eventually lead to diabetes mellitus. Finally the neurological and psychological changes that can occur are usually minor but development of psychological and intellect can sometimes be deficient (Dabelea and Pettitt 2008). Potential problems that may arise with the fetus from an exposure to maternal diabetes include abnormal organ mass, altered angiogenesis and increased levels of fetal insulin (Fetita 2006). It has also been found that if there is an increase in weight during pregnancy then there is usually a higher birth weight of the fetus (Humphreys 1954 cited in Catalano 2008 Chapter 11). The developing fetus cannot synthesise glucose and is dependent on the mother to produce it where it is transported to the fetus via facilitated diffusion through the placenta (Aerts et al 1996 cited in Mello, Parretti and Hod 2008). The result of decreased insulin sensitivity is that there is more glucose available to the developing fetus which can lead to a greater birth weight (Mello, Parretti and Hod 2008). Using animal models, it has been shown that exposure to high levels of glucose in utero can lead a diminished number of nephrons in the offspring (Amri et al 1999 cited in Fetita 2006 ref 68). This is important as nephrogenesis only occurs in the fetus and stops after birth (Gomez, Norwood 1999). It has been shown that a reduction in the numbers of nephron may affect the rate of progression of renal disease in adults due to an inability to secrete sodium. This may later develop into salt-sensitive hypertension (Brenner et al 1988). The mechanisms of reduced organ mass, high levels of fetal insulin and defects in angiogenesis may help explain how the fetus programs abnormal glucose tolerance in adulthood as a result of exposure to GDM (Fetita 2006). Transmission of diabetes from mother to offspring Exposure to gestational diabetes mellitus increases the risk of the fetus developing abnormal glucose tolerance which may develop into type 2 diabetes. (Fetita et al 2006). The association between greater incidences of the offspring having diabetes with a mother with GDM is greater than what would be predicted that could be passed on by maternal genetics (McLean et al 2006). One study showed that the phenotype for GDM/T2D was more common in daughters of mothers who were diabetic rather than daughters