Epidemic Influences

Genetic research of obesity was partly successful in establishing obesity in model organisms – rodents where obesity occurs spontaneously together with other pathological aspects (insulin resistance, …). The main cause of monogenic obesity in these model organisms are common mutations always present in only one gene. Results of research on model organisms allowed us to understand biological mechanisms of calorie intake and regulation and maintenance of body weight. The most important insight into obesity was achieved in 1994 after discovery of ob gene encoding for leptin. In two years period, using screening method, candidate homologous genes, selected on genetic study basis on mice, another five genes were identified. Mutations on these genes were found to be the cause of autosomal recessive or dominant monogenic obesity. Products of these genes are leptin and its receptor, proopiomelanocortin (POMC) melanocortin receptor 4 (MC4R) and

Although the mechanism of obesity development is not fully understood, it is confirmed that obesity occurs when energy intake exceeds energy expenditure. There are multiple etiologies for this imbalance, hence, and the rising prevalence of obesity cannot be addressed by a single etiology (Dehghan et al., 2005, p.

instrument of the advancement of obesity is not fully recognized and it is understood to be a

After breaking down the components of the biopsychosocial model in respect to childhood obesity, the literature contained some strengths and weaknesses. In the past, heredity and environmental factors were known to operate separately, however research indicates that genes affect psychological and social factors, promoting the biopsychosocial model. The Human Obesity Gene Map, published in 1994 provided research regarding the origin of obesity to mutations in genes, disorders, obesity phenotypes, or heredity. This collection of specific genes is annually updated and provides current information regarding obesity. This is a strength to the ongoing research of the etiology of obesity and how it may cause other

The hormone Leptin containing a malfunction is one of the causes for Monogenic Obesity, among many others. Leptin is a hormone that helps regulate body fat and also helps in parts of the brain that controls hunger and tells the body when it’s full. When the Leptin hormone is shortened or absent the body doesn’t secrete fat, but rather stores it making a person become obese. In 1997, two Pakistani cousins were reported with extreme obesity, “Both children had undetectable levels of serum leptin and were found to be homozygous for a frameshift mutation in the LEP gene (ΔG133), which resulted in a truncated protein that was not secreted.” (endocrine.org) In other words, the children contained two types of the same gene whether it be dominant or recessive that were either inserted or deleted causing the levels of the Leptin hormone to be shortened. After the findings of the two Pakistani cousins, there have been five more cases reported with children that lack the leptin hormone, which are all of Pakistani descent, but not related to each other. There has only been one case reported that was found in an Algerian family of three siblings in which the leptin receptor was found abnormal were one was joined to the other allowing a mutated one to work causing there to be more Leptin hormones than there needed to

Many studies have shown that high VF is significantly related to insulin resistance [11]. Normal weight individuals with low subcutaneous fat, but increased VF had greater insulin resistance than those with lower VF [8]. When evaluating this relationship in obese, metabolically at risk obese had more VF and greater insulin resistance than MHO [5]. On the other hand, subcutaneous fat seems to be associated with increased levels of leptin [11], a hormone secreted by adipose tissue that signals the amount of energy stores (fat mass) available in the body [12]. Leptin levels are positively correlated with FM [12], with obese individuals exhibiting high leptin concentrations [11]. Since obese individuals have an excess of body fat, high concentrations of leptin should decrease energy intake and increase energy expenditure which would promote a return to normal weight. Despite the potential physiological function, the role of leptin in energy expenditure is not completely understood. Research has demonstrated obese individuals to have high

The broken down food contains nutrients that activates the G-protein coupled receptors of enteroendocrine cells (Sam et al, 2012). On activation, it releases a number of gut hormones which passes the nutrient availability signal to the hypothalamic arcuate nucleus (ARC). This ARC is known to mediate intake of food and energy expenditure. (Peruzzo et al, 2000; Schaeffer et al, 2014; Sainsbury et al, 2010). Several circulating peptides: insulin and leptin are responsible for adiposity and energy deposits. ARC has two neural populations that act antagonist to each other. The medial part contains orexigenic neurons that regulate neuropeptide Y (NPY) and agouti-related protein (AgRP). The lateral part acts as an anorexigenic neurons expressing alpha-melanocyte-stimulating hormone (a-MSH) formed from pro-opiomelanocortin (POMC) and cocaine-amphetamine regulated transcript (CART) (Hahn et al, 1998; Elias et al,

Describe the role of ghrelin in food intake regulation and its involvement in development of obesity.

Moving from a genetic predisposition to obesity itself usually requires an adjustment in an individual’s eating habits, regime, or other environmental factors. Having a better grasp of what contributes to the genetics of obesity, especially common obesity-and gene-environment relations, will produce a better understanding of the pathways that lead to obesity. Such data could someday produce favorable tactics for obesity treatment and prevention. But it’s imperative to remember that generally, the impact of genes to obesity possibility is minor, while the influence of our activity environment and toxic food is enormous. As one scientist wrote, “Genes may co-determine who becomes obese, but our environment determines how many become obese.” (20) Which is why obesity prevention efforts must be at the forefront on changing our environment to make healthier choices and stress-free choices, for

The study design is broken down into two phases; phase one is to identify and extract literature that focuses on gene-encoding proteins involved in the link between obesity and diabetes. Once these gene-encoding proteins are identified, the sequences, in FASTA format, are extracted from the National Center for Biotechnology Information (NCBI). Phase 2 then analyzes those genes by utilizing the Multiple Sequence Alignment provided by the ClustalW tool found online. With the sequence aligned phylogenetic tress and alignment scores can be visualized for better analysis of potential homologies. Results identify seventeen proteins one of them being resistin; resistin has a number factors that contribute to obesity including the increase in fatty acid and adipocytokine levels. This is important because adipocytokines have been linked to the development of insulin resistance. Resistin has been thoroughly studied in regards to the link it plays in obesity and diabetes. One study that this article highlights is that insulin, FFAs, and TNF-a (known resistin inhibitors) are increased in obesity, however, this statement contradicts other studies performed in human and rodent students making resistin a controversial protein linking obesity and diabetes. Other gene-encoding proteins that have been linked to obesity and diabetes are ADIPOQ, MAPK8, and ICAM1.

However, it is possible that the metabolic changes associated with obesity are implemented in the relationship between obesity and adiponectin. For example, insulin resistance and hyperinsulinemia are frequently associated with obesity, and both decline with weight loss (Abbasi et al., 2004). Our results demonstrate that serum adiponectin levels significantly negatively correlated with BMI and non significantly negatively correlated with WC. Adiponectin has consistently been found to be negatively correlated with obesity in previous studies (Baratta et al., 2004). However, other studies did not find significant correlation (Kuo and Halpern,

Body weight, food intake and metabolism are regulated by the hypothalamus that processes central and peripheral signals. Within the hypothalamus, neurons residing in the ARC (arcuate nucleus) – PVN (paraventricular) –PF/LH (perifornical/lateral hypothalamus) axis communicate with each other and are subjected to the influence of several peripheral factors, including leptin and insulin (Davis et al. 2010). The action of these hormones on food intake occurs in part by convergence on a specific set of neurons within the ARC (Elmquist et al. 1998, Abizaid & Horvath 2008) that contains neuronal populations expressing orexigenic neuropeptide Y (NPY) and agouti-related peptide (AgRP) and the anorectic pro- opiomelanocortin (POMC). NPY synthesis and secretion have been found

To look at the involvement of canonical insulin/PI3K/Akt pathway in adipocytes leptin secretion the study measured it using insulin resistant DIO mice with HFD and CD fed mice, with the HFD mice gaining higher body and fat mass. Cell lysate of both HFD and CD fed mice were subjected to western blotting and it was observed that phospho-Akt level in adipocytes from HFD fed mice was lower than the CD fed mice after insulin stimulation, showing insulin resistance in the HFD fed mice. Also, the fasting leptin level of HFD fed mice is ten times higher than the CD fed mice. Refeeding, resulted in no significant increase in plasma leptin levels in HFD fed mice after two hours, whereas with the CD fed mice there was a significant increase in plasma leptin levels. This implies that leptin production and/or secretion after refeeding is impaired in HFD fed mice. To verify that there is a decrease in systematic leptin level, the researchers isolated primary adipocytes from HFD and CD fed mice and then determined ISLS in ex vivo. The result was that ISLS was significantly lower in primary adipocytes from HFD fed mice. This supports the hypothesis that impaired ISLS in HFD fed mice in vivo and ex vivo was dependent on PI3K/Akt activation. Furthermore, there is an essential role of PI3K/Akt in regulating ISLS in primary adipocytes as seen when blocking PI3K activity with wortmannin. This significantly inhibits ISLS without affecting basal leptin secretion. Also, AKT 1/2 inhibitor Akti

Obesity is a complex multifactorial disease caused by genetic and epigenetic factors, among others. An adverse intrauterine environment, like excess or restrict diet, can lead the fetus to develop metabolic syndrome, type 2 diabetes, and cardiovascular disease when its grow up. These complications pass through family’s descendants as a result of epigenetic modifications. Physical activity is a non-pharmacology form of prevention and treatment of obesity, and it helps to improve cardiorespiratory fitness and body composition, beside other elements. For this reason, this study evaluated whether or not a high sugar/high fat (HS/HF) diet would affect anxiety levels and memory patterns of female Wistar rats from generation F0, and if these changes

There are many hormones involved in diet control, only a few will be discussed. Leptin is a hormone secreted from adipose (fat) tissue. The more adipose tissue, the more leptin is secreted and acting on the Hypothalamus, signals the body to refrain from eating more – thus we becomes less hungry. Ghrelin, another hormone, is secreted mostly from stomach cells. Its secretion is intensified when there is little food in the gastro-intestinal