Thursday, June 6, 2013

Hormones and Body Weight

Excessive intake of calories in relation to energy expenditure over a long period of time results in body weight gain.

A complex physiologic system regulates energy homeostasis by integrating signals from peripheral organs with central coordination in the brain. The hypothalamus functions as the main cerebral center in which these signals converge.


Some of the important hormones involved in signaling are:
Fig. Functions of Leptin, Ghrelin, Insulin and PYY

Long term Signal

Leptin

Leptin is a small protein (167 amino acids) that is produced in adipocytes and moves through the blood to the brain, where it acts on receptors in the hypothalamus to decrease appetite.
Leptin is produced proportionally to the adipose mass and thus informs the brain of the fat store level. Leptin carries the message that fat reserves are sufficient, and it promotes a reduction in fuel intake and increased expenditure of energy. Leptin receptor interaction in the hypothalamus alters the release of neuronal signals to the region of the brain that affects appetite.

Leptin also stimulates the sympathetic nervous system, increasing blood pressure, heart rate and permits continual oxidation of fatty acids in an adipocyte without ATP synthesis, dissipating energy as heat  (thermogenesis ) and consuming dietary calories or stored fats in potentially very large amounts.

Insulin

Insulin acts on insulin receptors in the hypothalamus to inhibit eating and therefore decrease fuel intake and increase thermogenesis. Insulin  also signals muscle, liver, and adipose tissues to increase catabolic reactions, including fat oxidation, which results in weight loss.

Fig. Hormones that control eating

Adiponectin

Adiponectin is a peptide hormone (224 amino acids) produced almost exclusively in adipose tissue. It circulates in the blood and powerfully affects the metabolism of fatty acids and carbohydrates in liver and muscle.

Function of adiponectin
- increases the uptake of fatty acids from the blood by muscle cells
- increases the rate at which fatty acids undergo β oxidation in the muscle
- It also blocks fatty acid synthesis and gluconeogenesis in hepatocytes,
- it stimulates glucose uptake and catabolism in muscle and liver.

Study in mice with defective adiponectin genes are less sensitive to insulin than those with normal adiponectin, and they show poor glucose tolerance; ingestion of dietary carbohydrate causes a long-lasting rise in their blood glucose. These metabolic defects resemble those of humans with type II diabetes, who also are insulin insensitive and clear glucose from the blood only slowly. Indeed, individuals with obesity or type II diabetes have lower blood adiponectin levels than nondiabetic controls.

Short-term signals (Ghrelin, peptideYY)

Short-term signals from the gastrointestinal tract control hunger and satiety, which affect the size and number of meals over a time course of minutes to hours. In the absence of food intake (between meals), the stomach produces ghrelin, appetite-stimulating hormone that drives hunger. During a meal, as food is consumed, gut hormones, including cholecystokinin (CCK) and peptideYY (PYY), among others, through actions on the gastric empyting and neural signals to the hypothalamus, cause satiety and meals are terminated. Glucagon-like peptide–1 (GLP-1) derived from pre-proglucagon and secreted upon food ingestion by the proximal gastrointestinal tract, exerts pleiotropic effects, including slight anorexic effects.


Long-term and short-term signals interact and produce resultant effect in the body.

(Source: lehninger 4th Edition, Lippincott's Illustrated Reviews : Biochemistry)
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