Free Essay About Maternal And Offspring Obesity
There are several hypotheses and theories that suggest that the occurrence of maternal obesity has adverse outcomes for the offspring’s health in the later life. Human and animal studies have shown evidence that indicate that obesity in mothers increases the offspring’s risk of developing obesity. With the varied evidence, it is necessary for maternal obesity is curbed in the bud to lower the risk of offspring becoming obese in their later lives.
Maternal obesity or excessive maternal nutrition may lead to obesity and obesity-related disease in offspring later in life. Overweight or obesity is an accumulation of excessive fat, and this impedes health, relating to cardiovascular disease, diabetes, etc. Approximately 68% of the adult population is considered overweight, and one-half of this group is obese (Zambrano, & Nathanielsz, 2013). Maternal over-nutrition impacts on appetite regulation and the hypothalamus in developing foetus, which leads to increased adipose storage. Appetite stimulators; the agouti- related protein (AgRP) and the neuropeptide Y (NPY) in the ARC are increased, while POMC and a- MSH levels are decreased in the foetus. A key pathway of foetal programming includes those mediated through glucocorticoids and 11BHSD in the regulation of adipose tissue, which is associated with metabolic syndrome in adulthood and obesity.
The following paper will discuss the programming of appetite regulation and the hypothalamus specific to the developing foetus and development of programming of foetal programming of adiposity (Nathanielsz, Ford, Long, Vega, Reyes- Castro, & Zambrano, 2015), as well as a key pathway of foetal programming include those mediated through glucocorticoids and 11BHSD in the regulation of adipose tissue, which interrelates to metabolic syndrome in adulthood and obesity. Current methodologies used in the treatment of obesity will be discussed (Kathleen, Raleigh, Joshua, & Endla, 2009).
Maternal over-nutrition and obesity influences an offspring’s potential for developing obesity and related disease in later life. An example of this is the impact on appetite regulation and the hypothalamus in developing foetus, which leads to increased adipose storage. An increased risk of developing diabetes, obesity, hyperglycaemia, hyperinsulinemia and metabolic syndrome occur later in life. The foetus in uterus receives its nutrition entirely by trans- placental transfer from the maternal circulation (Ojha, Budge, 2012). This includes glucose, glucocorticoids, free fatty acids, glucose and amino acids which cross the placenta and into the foetus. The maternal insulin does not however cross this barrier and is not transferred to the child. The developing foetus responds to the glucose by producing additional insulin via its own pancreas. This hormone acts as a growth hormone and increases levels of adiposity. An increased level of glucose concentrations in the foetus results in hyperglycaemia, hyperinsulinemia and macrosomia. This will result in a higher risk of developing obesity and type two diabetes for the offspring (Nathanielsz, Ford, Long, Vega, Reyes- Castro, & Zambrano, 2015).
According to Muhlhausler, Adam, Findley, Duffield, & McMillen (2006), the arcuate nucleus of the hypothalamus is an aggregation of neurons in the hypothalamus, which receives and forms signals from peripheral hormones such as leptin and insulin. Leptin has a role in the inhibition of hunger via signals to the hypothalamus while insulin promotes absorption of glucose. Although leptin acts as an inhibiting hormone, excessive levels produced by adipogenesis, tend to be not sensitive to effects of leptin. The mediation of energy balance and apetite control is done by a collection of hypothalamic neuropeptides that are usually expressed in the hypothalamus’ arcuate nucleus (ARC). Appetite regulators are neuropeptide Y (NPY) and agouti- related protein (AgRP). Postnatal over nutrition leads to downregulation of NPY, increased expression of POMC mRNA inside the ARC and downregulation of hypothalamic glucose transporter (GLUT) 4 and mTOR expression. This occurs in response to increased energy stores signals, including glucose, insulin and glucose. Agouti-related protein (AGRP) is co- expressed with NPY and acts as an antagonist for hypothalamic melanocortin receptors and an AGRP expression increase hence constrains the signaling of melanocortin and at the same time increases appetite (Kathleen, Raleigh, Joshua, & Endla, 2009). The offspring has a reduced expression of leptin receptor (ORBb) expression in the hypothalamus ARC. This is associated with increased levels of adiposity. Increased adiposity is associated with reduced expression of leptin receptors in the ARC, and this is associated with a decreased sensitivity to the actions of leptin. The network is chiefly regulated by the adipocyte-derived hormone leptin, whose receptor is expressed on the neurons within the appetite-regulating network (Ojha, Budge, 2012). The developing foetus is no longer able to appropriately regulate its appetite in response to an increase in fat deposition, and this appears to be a consequence of reduced expression of the leptin receptor in the appetite-regulating centre. Consequently, a high maternal weight is associated with a higher risk of gestastional diabetes mellitus, which exposes the foetus to further risks due to hyperglycaemia, and hyperinsulinemia during development.
The nutritional environment that the offspring is exposed or subjected to during both the prenatal as well as the perinatal development usually has consequences in the long term when it comes to the functionality of the neural network of appetite regulation; and this has a clear impact on the regulation of an infant’s energy balance, feeding behavior, as well as body weight in later life (Muhlhausler, Adam, Findlay, Duffield, & McMillen, 2006). While maternal over-nutrition and obesity impact foetal appetite regulation and hypothalamus, excess glucocorticoid release also alters the appetite and increases adiposity (Spencer, & Tilbrook, 2010).
An excessive glucocorticoid release correlates to an altered appetite regulation and metabolism, which increases adiposity in foetal development. There is a significant correlation to high levels of glucocorticoid release and fat accumulation. Glucocorticoid receptors (GRs) are situated in visceral adipose tissue, as well as 11B- hydroxysteroid dehydrogenase type one. Overexpression of the (11BHSD1) and glucocorticoids causes fat accumulation, hypertrophy, increased lipolysis, increased lipoprotein lipase and hyperplasia. Glucocorticoids also stimulates the release of non-esterified fatty acids from adipocytes through activation of hormone- sensitive lipase, the enzyme that enhances fatty acid mobilisation. This increase in circulating free fatty acids may restrict glucose utilisation and encourage insulin resistance. Glucocorticoids also enhance lipid metabolism through its effect on both the turnover and uptake of fatty acids in adipose tissue, as well as up- regulate NPY Y2 receptor in abdominal fat, leading to stimulation of proliferation and differentiation of adipocytes, which leads to fat accumulation (Spencer, & Tilbrook, 2010).
Hypertrophied cells normally alter the adipose tissue-resultant adipokines and cytokines balance leading to a state of proinflammation, therefore performing as a crucial factor that associates obesity or overweight to the development of the metabolic related diseases in the child and the mother. These inflammatory mediators that include the interleukin-6 (IL-6) and the C-reactive protein (CRP are elevated systemically in instances of obesity in the developing foetus (Desai, & Ross, 2011). Maternal over nutrition during the late gestational period programmes and increased mRNA expression of PPAR-γ, lipoprotein lipase (LPL), adiponectin, and leptin in foetal perirenal fat. Glucocorticoids stimulate food intake by interacting with several appetite-regulating targets. They increase AMP-activated protein kinase signalling the ARC to start up-regulating AGRP and NPY expression in this particular region as well as stimulate these orexigenic peptides' actions. Acutely, glucocorticoids stimulate insulin secretion from the pancreas leading to appetite-suppression. However, it is important to note that chronically activated glucocorticoids also play part in insulin secretion (Torres, & Nowson, 2007).
Current methodologies used in the treatment of maternal related obesity include attempts to maintain glycaemic control through diet. Ensuring low glycaemic index diets is significant because carbohydrates are digested slower while releasing glucose gradually into the bloodstream. A low glycaemic index diet improves insulin sensitivity and assists with maintenance of weight loss. This intervention will assist in reducing obesity and diabetes in the offspring. The methodologies that are pursued in treatment also involve combining diet with changes to sedentary lifestyles (Reilly et al., 2002). Obesity is a lifestyle disease that mainly emanates from consumption of junk foods with excessive amounts of energy, salt, sugar, and fat. To counter the disease requires several interventions to one’s lifestyle. Many of the lifestyle interventions are aimed at increasing the physical activity. These interventions include reducing time spent watching TV, cycling, taking walks (Fontaine and Barofsky, 2001). Such activities ensure that people stay active and utilize any excess sugar and fat in their bodies through sweat hence eliminating the possibility of accumulation of sugar and fat in the body. Moreover, consuming a balanced diet that is free from excess fat, sugar, salt is also necessary for the prevention of obesity development. There is evidence that a combination of exercise and diet is crucial in reducing the risk of developing obesity. Additionally, brown adipose tissue from human fat in recent days is being targeted in developing anti-obesity therapies (Cypress and Kahn, 2010). These therapies increase of energy expenditure in the body. The brown adipose tissue has a good thermogenic capacity hence can be used to induce weight loss by initiating expenditure of energy.
In conclusion, maternal obesity correlates to obesity-related disease in offspring later in life. Overweight or obesity impedes health, via an increased risk of obesity and diabetes. Maternal over nutrition impacts on appetite regulation and the hypothalamus in developing foetus, which interrelates to increased adipose storage. Here, the appetite stimulators; neuropeptide Y (NPY) and agouti- related protein (AgRP) in the ARC are increased, while POMC and a- MSH levels are decreased in the foetus. (Nathanielsz, Ford, Long, Vega, Reyes- Castro, & Zambrano, 2015). Current methodologies used in the treatment of obesity include attempts to maintain glycaemic control through diet. Studies that explore the link between maternal obesity and the development of obesity in offspring in the later years are important in presenting evidence that support this phenomenon. Knowledge of the factors that result in the occurrence of this phenomenon will be important in helping mothers prevent obesity thus ensure that they give birth to children who are free from the risk of developing obesity. As observed in the preceding discussion, the prevention of obesity involves a combination of diet and exercise as well as a couple of other therapies.
Bayol, S. A., Farrington, S. J., & Stickland, N. C. (2007). A maternal ‘junk food ‘diet in
pregnancy and lactation promotes an exacerbated taste for ‘junk food ‘and a greater propensity for obesity in rat offspring. British Journal of Nutrition, 98(04), 843-851.
Cypess, A. M., & Kahn, C. R. (2010). Brown fat as a therapy for obesity and diabetes. Current opinion in endocrinology, diabetes, and obesity, 17(2), 143.
Drake, A. J., & Reynolds, R. M. (2010). Impact of maternal obesity on offspring obesity and cardiometabolic disease risk. Reproduction, 140(3), 387-398.
Fontaine, K. R., & Barofsky, I. (2001). Obesity and health‐related quality of life. Obesity reviews, 2(3), 173-182.
Mingrone, G., Manco, M., Mora, M. E. V., Guidone, C., Iaconelli, A., Gniuli, D., & Ghirlanda, G. (2008). Influence of maternal obesity on insulin sensitivity and secretion in offspring. Diabetes care, 31(9), 1872-1876.
Reilly, J. J., Wilson, M. L., Summerbell, C. D., & Wilson, D. C. (2002). Obesity: diagnosis, prevention, and treatment; evidence based answers to common questions. Archives of Disease in Childhood, 86(6), 392-394
Shankar, K., Harrell, A., Liu, X., Gilchrist, J. M., Ronis, M. J., & Badger, T. M. (2008). Maternal obesity at conception programs obesity in the offspring. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 294(2), R528-R538.