Abstract
Glucocorticoids are stress hormones that modulate a large number of physiological actions involved in metabolic, inflammatory, cardiovascular and behavioral processes. The molecular mechanisms and the physiological effects of glucocorticoids have been extensively studied. However, the involvement of glucocorticoid action in the etiology of the Metabolic Syndrome has not been well appreciated. Recently, accumulating clinical evidence and animal genetics studies have attracted growing interest in the role of glucocorticoid action in obesity and insulin resistance. This review will discuss the metabolic effects in the context of glucocorticoid metabolism and establish the association of glucocorticoid action with the features of the Metabolic Syndrome, especially obesity and insulin resistance. Special discussions will be focused on corticosteroid-binding globulin and 11β-hydroxysteroid dehydrogenase type 1, two proteins that mediate glucocorticoid action and have been implicated in the Metabolic Syndrome. Due to the complexities of the glucocorticoid biology and the Metabolic Syndrome and limited space, this review is only intended to provide a general link between the two areas with broad rather than in-depth discussions of clinical, pharmacological and genetic findings.
Highlights
Insulin resistance and hyperinsulinemia are often associated with a group of risk factors such as obesity, dyslipidemia, hypertension and impaired glucose tolerance
The point of view became institutionalized and the National Cholesterol Education Program's Adult treatment Panel III (ATP III) and the World Health Organization (WHO) have slightly different definitions [4,5,6], the Metabolic Syndrome is consistently characterized by a collection of metabolic abnormalities such as insulin resistance, obesity, dyslipidemia, hyperglycemia, and hypertension [7]
The prevalence of the Metabolic Syndrome is more than 20% among the US adults adjusted for age [8], which is far greater than observed in an earlier study with European participants at least partly due to
Summary
Insulin resistance and hyperinsulinemia are often associated with a group of risk factors such as obesity, dyslipidemia, hypertension and impaired glucose tolerance. Despite the compensatory response by the HPA axis to balance the plasma free cortisol or corticosterone concentrations under conditions of CBG reduction or deficiency, http://www.nutritionandmetabolism.com/content/2/1/3 tissue-specific GC excess can still occur This is especially important with respect to GC-stimulated differentiation of pre-adipocytes and insulin resistance of mature adipocytes, with the former effect increasing fat content and the latter reducing the tissue sensitivity to insulin. Selective overexpression of 11β-HSD1 in liver only caused mild insulin resistance with no effect on fat depot mass [153], impaired hepatic lipid clearance and hypertension were observed in these animals These transgenic studies demonstrate that both the hepatic and adipose 11β-HSD1 activities contribute in some way to insulin resistance and other features of the Metabolic Syndrome. Liver selective targeting of the drug appears to be a good strategy [180]
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