Abstract
Women have more body fat than men, but in contrast to the deleterious metabolic consequences of the central obesity typical of men, the pear-shaped body fat distribution of many women is associated with lower cardiometabolic risk. To understand the mechanisms regulating adiposity and adipose tissue distribution in men and women, significant research attention has focused on comparing adipocyte morphological and metabolic properties, as well as the capacity of preadipocytes derived from different depots for proliferation and differentiation. Available evidence points to possible intrinsic, cell autonomous differences in preadipocytes and adipocytes, as well as modulatory roles for sex steroids, the microenvironment within each adipose tissue, and developmental factors. Gluteal-femoral adipose tissues of women may simply provide a safe lipid reservoir for excess energy, or they may directly regulate systemic metabolism via release of metabolic products or adipokines. We provide a brief overview of the relationship of fat distribution to metabolic health in men and women, and then focus on mechanisms underlying sex differences in adipose tissue biology.
Highlights
Women have more body fat than men, but in contrast to the deleterious metabolic consequences of the central obesity typical of men, the pear-shaped body fat distribution of many women is associated with lower cardiometabolic risk
Because excellent reviews of sex differences in the regulation of food intake and body weight have been recently published [6,7], in this review, we focus on physiologic and genetic determinants of sex differences in fat distribution
Sex differences in the fat phenotypes are probably determined by a complex interplay of genetic, epigenetic, and hormonal factors
Summary
Sex differences in the fat phenotypes are probably determined by a complex interplay of genetic, epigenetic, and hormonal factors. Elegant in vivo studies of depot- and sexspecific differences in adipose tissue metabolism showed that the primary suspects (lipid uptake and mobilization) are not the main mediators and at the same time pointed to new pathways (direct FFA uptake) for further investigation. We still do not know if sex differences in the function of female adipocytes are mainly derived from genetic, cell autonomous properties related to sex chromosomes or from critical early imprinting events by sex steroids. The direct effects of sex hormones on adipocyte function and the importance of the microenvironment of specific adipose depots on growth remain poorly understood.
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