IPHREHAB : OBESITY ETIOLOGY

IPHREHAB

OBESITY 


AETIOLOGY
Obesity is a heterogeneous group of disorders.
Causes of obesity remain elusive 
At one level, the pathophysiology of obesity seems simple: a chronic excess of nutrient intake relative to the level of energy expenditure. 
Complexity of the neuroendocrine and metabolic systems  has been difficult to quantitate

GENES

Obesity is commonly seen in families.

Inheritance is usually not Mendelian,

Adoptees usually resemble their biologic rather than adoptive parents with respect to obesity

Likewise, identical twins have very similar BMIs whether reared together or apart, and their BMIs are much more strongly correlated

ENVIRONMENTS

It plays a key role in obesity, 

Famine prevents obesity in even the most obesity-prone individual. 

Recent increase in the prevalence of obesity in the United States is due to environments

Cultural factors are also important. Easy availability and composition of the diet 

Decreased physical activity. 

In industrial societies, obesity is more common among poor women, whereas in underdeveloped countries, wealthier women are more often obese. 

In children, obesity correlates to some degree with time spent watching television.

High-fat diets may promote obesity, as may diets rich in simple carbohydrates. 

CAUSES OF OBESITY

Cushing's Syndrome  Although obese patients commonly have central obesity, hypertension, and glucose intolerance

Hypothyroidism should be considered when evaluating obesity, but it is an uncommon cause

Insulinoma  Patients with insulinoma often gain weight to avoid hypoglycemia

Craniopharyngioma and Other Disorders Involving the Hypothalamus  

Tumors, trauma, or inflammation, hypothalamic dysfunction of systems controlling satiety, hunger, and energy expenditure can cause varying degrees of obesity

Leptin in Typical Obesity

The vast majority of obese people have increased leptin levels but do not have mutations of either leptin or its receptor.

"leptin resistance." Data suggesting that some individuals produce less leptin per unit fat mass than others or have a form of relative leptin deficiency that predisposes to obesity

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.