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Susan K. Fried, Andrew S. Greenberg, Lipocalin 2: A “Sexy” Adipokine that Regulates 17β-Estradiol and Obesity, Endocrinology, Volume 153, Issue 4, 1 April 2012, Pages 1582–1584, https://doi.org/10.1210/en.2012-1012
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Female mice, like premenopausal women, are generally protected from the insulin resistance and inflammation associated with obesity. With aging and menopause, levels of estrogens fall and women tend to gain body fat and become as susceptible as men to obesity-related metabolic diseases. In male mice, high-saturated-fat diets cause obesity, systemic insulin resistance, and adipose tissue inflammation, especially in gonadal fat depots where adipocyte death is associated with macrophage infiltration and activation. Female mice also gain body fat on high-fat diets, although they exhibit much lower levels of adipose inflammation and insulin resistance (1, 2). This sex difference is not likely entirely attributable to estrogens because high-fat feeding of ovariectomized female mice does not increase adipose death to levels seen in high-fat-fed males (1). Over and above female sex, a lower-body or gynoid fat distribution further protects women from metabolic disease (3). Thus, mechanisms linking the biology of specific fat depots to sex differences in metabolic risk are of great interest for translational research.
