Sunday 8 January 2012

IPHREHAB : OBESITY..REGULTAION

IPHREHAB


OBESITY.

PHYSIOLOGY
Body weight is regulated
  • Endocrinal Component
  • Neural components 
Small imbalances between energy intake and expenditure will ultimately have large effects on body weight. 
For example, a 0.3% positive imbalance over 30 years would result in a 9-kg weight. gain

NORMAL REGULATION
There is autoregulation weight
Weight loss increases appetite and energy expenditure falls 
With overfeeding, appetite falls and energy expenditure increases. 
This latter compensatory mechanism frequently fails in OBESE PERSONS, permitting obesity to develop when food is abundant and physical activity is limited. 

REGULATION-LEPTIN
Leptin is hormone which is a major regulator of these adaptative responses
It is the adipocyte-derived hormone
 Leptin, acts through brain circuits (predominantly in the hypothalamus) to influence appetite, energy expenditure, and neuroendocrine function

APPETITE CENTRE
Appetite centre is in the the hypothalamus Signals affecting on the hypothalamic are neural, hormonal , and metabolic. 
Vagal inputs are particularly important, bringing information from gut distention. 
Hormonal signals include leptin, insulin, cortisol, and cholecystokinin, which signals to the brain through the vagus nerve. 

Metabolites as glucose also  influence appetite.  Hypoglycemia  induces  hunger
The hormonal, metabolic, and neural signals  can act by influencing the expression and release of various hypothalamic peptides [neuropeptide} 

Psychological and cultural factors also play a role in the final expression of appetite. Apart from rare syndromes involving leptin, its receptor, and the melanocortin system the defects in this complex appetite control network that account for common causes of obesity are not well understood.


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