Climacteric obesity: from genesis to clinic

Gynecol Endocrinol. 2006 Jan;22(1):18-24. doi: 10.1080/09513590500453775.

Abstract

The etiology of obesity is multifactorial and still unclear. Genetic factors play a significant role and include several gene candidates: polymorphisms of genes for ss(2)-adrenoreceptor, resistin, estrogen receptor-a and peroxisome proliferator-activated receptor-gamma. Moreover, peptides regulating hunger and satiety, e.g. leptin, galanin, cholecystokinin and neuropeptide Y, and altered nutritional patterns have been implicated. Also, factors associated with aging, e.g. decreased levels of growth hormone and dehydroepiandrosterone, and the activity of the sympathetic nervous system (resting metabolism and thermogenesis) cannot be disregarded. Participation of the sex steroids and inflammatory factors has also been postulated in the etiology of obesity. Three phenotypes of obesity are postulated; however, the visceral (abdominal) phenotype is typical of postmenopausal women and is characterized by several metabolic disorders with high risks of diabetes mellitus type 2 and cardiovascular disease. On the basis of personal experience and data from evidence-based medicine, diagnostic-therapeutic algorithms of climacteric obesity are presented.

MeSH terms

  • Algorithms
  • Clinical Protocols
  • Female
  • Humans
  • Inflammation / complications
  • Obesity / etiology*
  • Obesity / pathology
  • Obesity / prevention & control
  • Perimenopause / genetics
  • Perimenopause / metabolism*
  • Postmenopause / genetics
  • Postmenopause / metabolism*
  • Subcutaneous Fat / pathology