Animal models of obesity--theories of aetiology

Baillieres Clin Endocrinol Metab. 1994 Jul;8(3):509-25. doi: 10.1016/s0950-351x(05)80284-8.

Abstract

The multiplicity of proposed mechanisms for obesity is confusing and many questions remain to be answered. A review of all the proposed mechanisms for obesity suggests that they can be placed in two groups (Table 3). The first centres on the role of the hypothalamus in the regulation of body weight. With further knowledge it may be possible to find unifying mechanisms originating in the brain for the set-point theory, the autonomic nervous system imbalance hypothesis, the thermogenesis, hyperphagia and the hyperinsulinaemia hypotheses and the gestational undernutrition hypothesis. This group of mechanisms suggests that obesity is due to altered function of central regulatory mechanisms and that the various related hypotheses are merely looking at different aspects of the same problem. The second centres on abnormalities intrinsic to the adipocyte and could link the fat cell and perinatal overnutrition theories. This group of theories suggests that an abnormality at the fat cell level, either genetic or acquired, can result in the excessive accumulation of fat. The two groups are not contradictory. The ability to develop obesity as a result of a fat cell abnormality does not negate the existence of regulatory central mechanisms since there is a finite capacity for these mechanisms to operate.

Publication types

  • Review

MeSH terms

  • Adipocytes / physiology
  • Animals
  • Autonomic Nervous System / physiopathology
  • Diet
  • Disease Models, Animal*
  • Energy Metabolism / physiology
  • Humans
  • Hyperglycemia / complications
  • Hyperinsulinism / physiopathology
  • Hyperphagia / complications
  • Hypothalamo-Hypophyseal System / physiopathology
  • Obesity / etiology*
  • Obesity / physiopathology
  • Pituitary-Adrenal System / physiopathology