Regional differences in triglyceride breakdown in human adipose tissue: Effects of catecholamines, insulin, and prostaglandin E2☆
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2020, Endocrinology and Metabolism Clinics of North AmericaCitation Excerpt :The only exceptions are adipocytes in the bone marrow, breast, and the epicardium; these adipocytes abut nonadipose tissue cells and thus can directly affect the function of adjacent cells independent of the circulation. The major adipose depots described above also differ in terms of the average size of the adipocytes,13 the responsiveness of the adipocytes to prolipolytic and antilipolytic hormones,15–17 the propensity of the adipocytes to take up and store fatty acids,18–20 as well as immune cell infiltration.21 The utilitarian rationale for defining human body fat compartments into lower-body fat, upper-body subcutaneous fat, and intraabdominal/visceral fat rests on the fact that the compartments can be measured using only dual-energy x-ray absorptiometry and a single-slice computed tomographic or MRI scan of the abdomen.22,23
The sexual dimorphism of obesity
2015, Molecular and Cellular EndocrinologyCitation Excerpt :Human fat cells express lipolytic β1–2 and antilipolytic α2-adrenergic receptors providing an additional mechanism to regulate lipolysis/lipogenesis and the filling of adipose tissues. A sexual dimorphism exists in the distribution of these receptors to account for sex- and depot-specific differences in the modulation of lipolysis (Richelsen, 1986; Richelsen et al., 1991). Estradiol increases α2-adrenergic receptors in subcutaneous adipose tissue but has no effect on adrenergic receptors in intraabdominal adipocytes (Pedersen et al., 2004).
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Supported by grants from NOVO, Nordic Insulin Foundation, the Danish Diabetic Association, P. Carl Petersens Fond, Aarhus University, and Danish Medical Research Council.