Involvement of Canonical Insulin

In wild type mouse there is no effect on food intake, body weight and blood glucose though we give more leptin because here the leptin receptors are constant. But, in ob/ob mouse the food intake, body weight and blood glucose levels are decrease because the presence of leptin receptor. However, in the db/db mouse there is no effect due to the absence of the leptin

In the paper “Activation of mTORC1 is essential for β-adrenergic stimulation of adipose browning” by Dianxin Liu et al, the authors sought to learn about the relationships between the opposing hormone regulating systems of adipocytes, Insulin and catecholamines, and their effects on the protein mTOR and its regulatory protein RAPTOR. These interactions may lead to discoveries that can ultimately help us enhance energy expenditure and combat metabolic disease. Adipose tissue depots perform a wide range of functions in the human body and consists mainly of two varieties, white adipose tissue (WAT) and brown adipose tissue (BAT). WAT stores extra caloric energy in the form of triglycerides, while BAT in direct contrast, rapidly converts oxidative energy into heat for survival in the cold. In addition, adipose depots also secrete proteins and other factors that are a part of energy metabolism and glucose homeostasis.

Insulin is a hormone that is produced in the pancreas to regulate the amount of glucose in the blood. The pancreas of an individual suffering from diabetes either does not produce insulin or only produces very little insulin. Before 1922 diabetes was a feared disease with no cure.

Insulin is a hormone that is produced from what is known as the “islets of Langerhans”, discovered by German Histologist Paul Langerhans, and is required for the utilization of glucose in muscle cells for energy. If the muscles are deprived of glucose for energy conversion, the muscles begin to utilize fat for energy (Roth). This however has toxic side effects, such as the production of high blood levels of Ketone bodies or otherwise known as Acetone. In high quantities, Acetone will accumulate in the blood, leading to brain damage and the possibility of brain death (Roth).

1994). Leptin is secreted primarily by adipocytes, proportionally to fat cell mass, and contributes to energy metabolism. Leptin will affect the energy balance by acting on the brain. Leptin can activate, directly or indirectly, specific centers in the hypothalamus to decrease food intake, to increase any energy expenditure, to influence the glucose, lipid metabolism, and alter neuroendocrine function (Campfield, Smith et al. 1995). Leptin resistance, in regards to obesity, was coined due to the increased leptin levels with no impact on regulating energy homeostasis. Leptin resistance causes insulin resistance and the accumulation of lipids is a direct result of the reduction of lipid oxidation in insulin-sensitive organs; shown in preclinical and clinical experiments with obese rodents and humans. However, the mechanisms that may lead to leptin resistance are still being researched (Mori, Hanada et al.

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You can ignore all the different angles and theories and focus on one thing: controlling insulin. Why is insulin so important? Because it ultimately controls how much fat you can lose.

What is type one diabetes? “With type 1 diabetes, the body’s immune system attacks part of its own pancreas” (“What is Type one diabetes” 1). The body is unable to function properly, resulting in unhealthy levels of high or low blood sugar. This will lead to dramatic consequences, if not treated quickly and correctly. Scientists are still not sure what is causing diabetes nor do they know how to stop it. There is still a lot that is unknown about type one diabetes. Type one diabetes is a terrible disease that can be controlled with proper precautions but most importantly, insulin.

After leptin is secreted by the adipose tissue, it enters the brain through the bloodstream. Gastric leptin may also reach hypothalamus through the vagal nerve and nucleus solitarius. Effects of leptin on various systems have been reported, including reproduction, immune system, hematopoesis, angiogenesis, bone formation and wound healing. It plays an important role in energy balance by inhibiting energy intake contrary to ghrelin, and by regulating body weight and energy homeostasis (Moran & Phillip, 2003).

Insulin also binds to IGF-1 receptors with low affinity (Smith, 1988) and stimulates the formation of an active Ras-GTP complex and ERK-MAPK pathway (Porras, 1996) and the PI3K pathway. Both these pathways appear to be required for adipogenesis (Sale, 1995; Sakaue, 1998; Tang, 2005). The Ras-GTP complex activates RAF kinase which is phosphorylated to induce MAPK. The phosphorylated MAPK interacts with Elk1. Phohosphorylation of Ekl1 facilitates binding to the mediator complex via the Med23 subunit (Stevens, 2002; Wang, 2005). The mediator complex is a multi-protein complex which bridges gene specific transcription factors and transcriptional machinery. The Mediator Med23 (Sur2) subunit was originally identified as a genetic suppressor of a hyperactive Ras phenotype in C.elegans (Singh, 1995). Elk1 is a member of the ternary complex factor family and an important regulator of adipogenesis. The Elk1/Med23 interaction controls the expression of Krox20 in a MAPK dependent manner by promoting a productive preinitiation complex which leads to transcription (Wang, 2009). Krox20 is expressed in adipose tissue (Soukas, 2001) and is the first transcriptional factor expressed during adipogenesis after insulin stimulation (Chen, 2005; Gonzalez, 2005). Krox20 expression has been reported to regulate

Incretins, are gut-derived hormones released predominantly by the L cells in the distal bowel in response to a meal. They reduce blood sugar concentrations by enhancing the insulin release from pancreatic beta cells and inhibiting postprandial glucagon secretion and gastric emptying after a meal (Hattori). Ghrelin, a peptide produced by the stomach, stimulates appetite and its levels increase with fasting and decrease after a meal (Cummings). It also has a pro-diabetic role, causing hyperglycemia through inhibition of insulin resistance and stimulation of release of counter-regulatory hormones, and impairing insulin sensitivity (Leite-Moreira). A peptide Obestatin, derived from ghrelin precursor but with opposite effects has recently been found to be produced by the same neuroendocrine cells that secrete the orexigenic hormone but counterbalances its effects by decreasing appetite (Zhang).

Insulin has been used for diabetes since 1922. “Leonard Thompson, a 14-year-old boy dying from diabetes in a Toronto hospital, became the first person to receive an injection of insulin” (“The History of a Wonderful Thing We Call Insulin” 1). Without insulin, thousands of people with diabetes would die. Insulin is available for people who need it because it was initially tested on animals. Oskar Minkowski and Joseph von Mering removed a pancreas gland from a dog in 1889, and it ended up dying later (“The History of a Wonderful Thing We Call Insulin” 1). Animals like dogs, have hormones in their blood so the experiment worked on them. It wasn’t safe for humans yet (Parry 1). Although putting an animal’s life at risk for medical research might

Very few cases of Metabolic Syndrome can be fully attributed to hereditary causes. Rather, over-time, an individual’s lack of proper lifestyle habits, including diet, physical activity, environmental health, stress, and interrupted sleep patterns, can lead to the formation of insulin resistance and the five conditions, eventually leading to Metabolic Syndrome. This is brought about by the invasion of white adipose tissue. Mononuclear cells release cytokines, which then create insulin resistance in various tissues including muscle and the liver. In fact, the American Heart Association states, “skeletal muscle is the primary tissue that accounts for glucose disposal.” (AHA) As a result of insulin resistance, glucose uptake and fat mass increase substantially. The reason for the uptake in glucose is due to the suppression of gluconeogenesis and glycogenolysis, which results in a decrease in glucose output from the liver. When these areas are lacking or have been neglected, the body physiologically responds by producing inflammation, which is the first line of immune defense of the innate immune

Insulin also stimulates glucose transport and the synthesis of triglycerides. Insulin helps prevent lipolysis which is the catabolic breakdown of triglycerides. Insulin also increases the uptake of fatty acids coming from circulating lipoproteins by stimulating lipoprotein lipase activity in fat tissue. Insulin resistance in obesity is shown by decreased insulin-stimulated glucose transport and metabolism in adipocytes by impaired suppression of hepatic glucose output. (Kahn, B., 2000) These defects may result from decreased insulin signaling and downregulation of GLUT4 which is the major glucose transporter that responds to insulin. In obesity, there is increased expression of several protein tyrosine phosphatases (PTPs), that dephosphorylate

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