Chapter 8

Menopause, Metabolic Syndrome and Diabetes Mellitus

Eleni I. Boutati and Sotirios A. Raptis


Industrialization across the 20th and 21st century has led to a greater than ever longevity and a smaller than ever birth rate. Because of female’s advantage in survival, a predominance of females achieving old age is observed globally. For first time in the human history, industrialized societies bear mounting burdens of chronic lifestyle-related diseases, such as obesity and type 2 diabetes (t2DM). In the contrary, ovarian follicle depletion leading to menopause has not be influenced by environmental factors and has been constant for centuries. The evolutionary origin of human menopause remains an enigma. The fact is that the human female reproductive system ages to the point of failure at a relatively young age, and thus it is not surprising to see a postmenopausal increase in the incidence of so many disorders above that expected by age alone. Metabolic syndrome (MS) could be characterized as the ''Pandora’s box'', due to its content and the surrounding debate concerning its clinical utility, keeps ultimately the importance of a cluster of cardiometabolic risk factors which identify individuals at high risk of both t2DM and cardiovascular disease (CVD). The evolutionary origins of the MS are debated. Insulin resistance, chronic inflammation and abdominal fat accumulation are thought to be implicated in its pathophysiology. CVD is the most common cause of mortality in women worldwide, but incidence in women lags behind men by 10 years. Normal aging and alterations of the hormonal milieu related to menopause contribute to changes in risk factors for CVD, such as visceral adiposity. Emerging evidence points to the adipose tissue as a crossroad in the development of the MS, inflammation and atherosclerosis. Underlying mechanisms involve disequilibrium between proinflammatory cytokines (high interleukin- 6/C-reactive protein) and the anti-inflammatory adipokine (low adiponectin).

Total Pages: 163-212 (50)

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