Abstract
Aging, like obesity, is associated with metabolic and inflammatory alterations within adipose tissue in older individuals. Younger females are protected from adipose inflammation, but older post-menopausal females exhibit exaggerated visceral adiposity correlated with increased disease risk. Obesity accelerates the onset and progression of age-associated diseases, but it is unclear if aging and obesity drive adipose tissue dysfunction in a sexually dimorphic fashion. We investigated adipose tissue metabolism and inflammation in a diet-induced obesity model in young and old mice. We identified age related sex differences in adipose tissue macrophages (ATMs), fibrosis and lipid metabolism in male and female visceral fat depot (GWAT). Although aging normalized body weights between the sexes, females remained protected from proinflammatory ATMs and stimulated lipolysis failed to adversely affect the inflammatory state even with obesity. Older obese males had augmented CD11c+ ATMs and higher insulin levels, while females showed increased visceral adiposity and exaggerated Pparγ, and Pgc1α expression. Obesity in aging demonstrated similar expression of GWAT p53, p16, p21, Timp1 and Tgfβ1 in both sexes. Our studies suggest that even with aging, female GWAT shows an attenuated inflammatory response compared to males due to an efficient oxidative metabolism combined with an active tissue remodeling state.
Highlights
Aging is associated with an increased risk for cardiovascular diseases, especially in older men and women [1, 2]
We investigated whether excess free fatty acid (FFA) accumulation with stimulated adipose tissue lipolysis by a β3-adrenergic receptor (ADRB3) agonist led to an additional varied inflammatory response in the older females
To assess sex differences in aging induced adipose tissue macrophage (ATM) induction we studied ATM profiles in the stromal vascular fraction (SVF) of gonadal white adipose tissue (GWAT) and inguinal adipose tissue (IWAT) from young (6 months) and old (10 months) male and female mice that were placed on normal diet (ND) or high fat diet (HFD) for 24-week
Summary
Aging is associated with an increased risk for cardiovascular diseases, especially in older men and women [1, 2]. Studies have shown that while young female mice have smaller infarcts after an experimental stroke compared to males, this phenotype is reversed in older animals [3]. The underlying mechanism behind this changed phenotype in aged females is unknown. One potential factor may be the age-related increase in adipose tissue in women during menopause, leading to increased adipose tissue inflammation and an enhanced systemic pro-inflammatory environment prior to the stroke. While some cardiovascular risk factors, such as heart disease, are more prevalent in younger men, the menopausal transition in women is associated with a significant increase in body weight and abdominal fat in older females [4]
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