Incretins In Bacteroidetes

(TCO 4) After a meal, which hormone is responsible for moving glucose into the body's cells?

They can either be hyperglycemic or hypoglycemic. Some early signs and symptoms of hyperglycemia are extreme thirst, weight loss, fatigue, headaches, trouble concentrating, blurred vision, and frequent urination. Later signs are dry mouth, fruity-smelling breath, shortness of breath, coma, confusion and fatigue. Glucagon is released overnight and between meals. Glucagon is important to balance the sugar and fuel. It signals the liver to break down its starch or glycogen stores and helps to form new glucose units and ketone units. Unfortunately, this does not occur in diabetics. Glucagon is being released during mealtime which is making the blood sugar increase. The liver is needing to make sugar because it is being produced during mealtime once again increases the blood sugar. If the blood sugar increases to quickly it will cause headaches, blurry vision and fatigue. The amylin has sub-normal amounts of GIP, and their beta cells don’t respond properly to GLP-1. This may explain why glucagon levels are not suppressed during a meal (Us,

acute effects of leptin on synaptic plasticity in the arcuate nucleus of the hypothalamus. The arcuate nucleus is one of the key targets of circulating hormones such as leptin. At least two distinct populations of neurons with opposing actions on food intake residein the arcuate nucleus, " (p.63). Pinto's data is ultimately described as helpful but also created many more questions, probably more than it answered.

The organs involved include the liver, muscle, fat cells, liver, alpha and beta cells of the pancreas, GI tract, kidney, and brain. While the liver and muscle ideally increase glucose uptake in the fed state when insulin levels are high, with type 2 diabetes this is impaired. To further exacerbate the hyperglycemic condition, the liver not only fails to properly exhibit glucose uptake, but it actually over produces more glucose and thereby creates a cycle of glucose accumulation and further production. While this is occurring in the muscle and liver, fat cells have accelerated lipolysis. The lipolysis results in an increase in plasma free fatty acids (FFAs), which then in-turn impairs both first and second phase insulin secretion and can lead to excess fat deposition in the liver and muscle, contributing further to impaired insulin production. At the GI tract, gastric inhibitory polypeptide becomes resistant and loss of GLP-1 occurs. With impaired GLP-1, insulin resistance is again further enabled and hyperglycemia can become more profound. This occurs because glucagon suppression from the pancreatic alpha cells post meal does not occur as it would under normal circumstances, thereby enabling even more hepatic glucose production. While theories are not completely conclusive, insulin resistance in the hypothalamus may contribute to excess intake thereby contributing to additional glucose in the circulation. Finally, the kidney also plays a role in glucose dysregulation as it increases glucose reabsorption. All of these discussed mechanisms ultimately contribute to hyperglycemia and chronic hyperglycemia itself contributes to impaired beta cell function (DeFronzo,

This is usually caused by a positive energy balance, and more relevantly a sedentary lifestyle. Increased amounts of visceral fat can be detrimental to the anti-inflammatory phenotype of adipose tissue, which is normally characterised by small adipocytes and the presence of anti-inflammatory immune cells, or adipokines, such as M2-macrophages and CD4-regulatory T-cells (Bishop et al., 2011). These cells release the anti-inflammatory cytokine adiponectin. The presence of visceral fat causes these adipocytes to expand, and then infiltrated by pro-inflammatory adipokines, such as M1-macrophages. This causes the secretion of pro-inflammatory cytokines, such as CRP and TNF (Bishop et al., 2011). These cause a state of low-grade systemic inflammation, which can cause vascular damage and disrupt regular metabolism (Canino et al., 2011)

Leptin and ghrelin are internal intermediary that affect feeding and appetite. Ghrelin is secreted by the stomach adjust short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is filled). Leptin is secreted by white adipose tissue to signal fat storage reserves in the body and mediates long-term appetitive controls (i.e. to eat less when fat storages are high and more when fat storages are low). It plays an efficient role in the regulation of energy balance and body weight by decreaing food intake and stimulating energy expenditure.39 Although, administration of leptin may be effective in a small subset of obese individuals who are leptin deficient. Most obese individuals are thought to be leptin resistant

Glucagon is the other hormone produced by the Islets of Langerhans. This hormone is produced by the alpha cells in the islets, which detect when blood sugar levels are too low (around 70 mg/dL) and respond by releasing glucagon. Glucagon stimulates the breakdown of stored glycogen into glucose through a process called glycogenolysis, and releases the glucose back into the bloodstream, thus raising blood sugar levels to a higher concentration. As blood glucose levels return to its equilibrium, the concentration of glucagon lowers until the time when glucose levels rise again. In reaction to this, insulin levels rise and fall with the levels of blood glucose concentration.

At its most basic, obesity results when individuals regularly take in more calories than needed. The body stores these excess calories as fat and over time the extra pounds add up. In theory, if fewer calories are taken in than the body burns, weight goes down. This equation can be deceiving, however and perhaps overly simple and there are always more factors at play. The role of gut bacteria in weight regulation is a topic that goes largely unmentioned when discussing factors related to obesity and weight loss, however it could hold answers as to why certain people are more prone to obesity or find it more difficult to lose

It has three sites involved in appetite regulation ventromendial nucleus, lateral hypothalamus and arcuate nucleus. Through studies using mice, lesions to the hypothalamus has resulted in hyperphagia or hypophagia. In human studies, patients with tumors in the hypothalamus have been shown to be hyperphagia or hypophagia. The regulation of food intake is a complicated process. It involves external factors and signals from certain hormones through the hypothalamus. These factors act as appetite stimulator and appetite suppressors to control energy intake and expenditure. There have been several weight loss drugs developed to treat obesity. Three of the drugs are orlistat, sibutramine, and rimonabant. Orlistat prevents fat digestions and absorption by binding to gastrointestinal lipases. The fat is blocked and fat is not digested and passed out in feces. Sibutramine works differently to affect the nerve cells in the brain that regulate appetite. Rimonabant works as a CB1 antagonist. The drug binds to a receptor without activating it and preventing endocannabinoid to bind to it which decreases cell signals for appetite. The desire is for less appetite. A person will gain weight once stopping the drugs and limited in there use for weight loss. Weight loss surgery is used to limit the amount of intake of foods by decreasing the size of the stomach. The options are the duodenal switch, gastric binding, sleeve gastrectomy and gastric

This resistance occurs when there is an increased concentration of insulin in the blood than needed to maintain blood glucose levels. The increased insulin in the blood is due to the increased glucose due to the cat consuming large amounts of food which is why the cat is obese in the first place. The insulin resistance then leads to pancreatic beta-cell dysfunction (Nelson and Reusch, 2014, and Hughston. 2014). These beta-cells are a major source for amylin secretion which is cosecreted with insulin to aid in maintenance in normal blood glucose by stimulating the breakdown of muscle glycogen (Lutz, 2008). Figure 1 demonstrates how obesity ties in with causes of

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).

either the paraventricular nucleus or acurate nucleus immediately decreases food intake in rats. NmU-R2 mRNA is expressed predominantly in the central nervous system and infact has been localized to the PVN and acurate nucleus in rat and. Effects of leptin on hypothalamic neuropeptide signaling and the effects on feeding and body weight have been documented previously for several other neuropeptides.

Reactive hypoglycemia, a rare form of hypoglycemia, increases insulin levels after the consumption of excess carbohydrates, leading to a drop in blood glucose levels. This differs from conventional hypoglycemia where blood glucose drops several hours after a meal, but can easily be returned to normal by the consumption of food. Reactive hypoglycemia can cause fatigue, dizziness, shakiness, and in extreme cases, a coma. Although no effective treatments exist, glucagon, a peptide hormone derived from pancreatic alpha cells, seems to reduce symptoms. In the proposed experiment, the effectiveness of glucagon relative to a regimen of dietary control, exercise, and Acarbose will be tested on Zucker-diabetic-fatty (ZDF) rats (Rattus rattus). Three

Ghrelin has largely been implicated in the research on prevention and treatment of obesity because of its role in GH secretion and appetite regulation. It has been demonstrated by many studies, that obese individuals have a marked decrease in GH secretion. Since GH is a hormone involved in many metabolic processes, low levels of GH could have significant effects on how the body is able to process food and store nutrients. Studies have found that an inverse correlation exists between BMI and both GH and ghrelin levels (McKibben,

The protein leptin is produced in response to satiation which is secreted into the bloodstream from fat tissue, leading to fat loss and decreased appetite. To support the role of this protein, Zhang et.al injected two copies of the gene for obesity into some mice and these ob/ob mice had a tendency to overeat. They discovered that the ob/ob mice had a defective gene for the protein leptin and were unable to experience a decrease in appetite as well as fat loss. However, injecting these mice with leptin caused them to lose weight dramatically. This shows how proteins also have a role in controlling our eating behaviour and not only neural mechanisms.