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)
No comments:
Post a Comment