Why the study?
Does caloric restriction ameliorate age-associated insulin resistance and inflammation in different adipose tissue depots in Wistar rats?
Does caloric restriction ameliorate age-associated insulin resistance and inflammation in different adipose tissue depots in Wistar rats?
This study demonstrates the differential susceptibility of various adipose depots to age-associated insulin resistance and inflammation, and highlights the protective effects of caloric restriction.
Answers are grounded in this paper and cite their sources.
Caloric restriction may mitigate age-related adipose inflammation in rats; hypothesis-generating for human depot-specific interventions.
The prevalence of insulin resistance and type 2 diabetes increases with aging and these disorders are associated with inflammation. Insulin resistance and inflammation do not develop at the same time in all tissues. Adipose tissue is one of the tissues where inflammation and insulin resistance are established earlier during aging. Nevertheless, the existence of different fat depots states the possibility of differential roles for these depots in the development of age-associated inflammation and insulin resistance. To explore this, we analyzed insulin signaling and inflammation in epididymal, perirenal, subcutaneous, and brown adipose tissues during aging in Wistar rats. Although all tissues showed signs of inflammation and insulin resistance with aging, epididymal fat was the first to develop signs of inflammation and insulin resistance along aging among white fat tissues. Subcutaneous adipose tissue presented the lowest degree of inflammation and insulin resistance that developed latter with age. Brown adipose tissue also presented latter insulin resistance and inflammation but with lower signs of macrophage infiltration. Caloric restriction ameliorated insulin resistance and inflammation in all tissues, being more effective in subcutaneous and brown adipose tissues. These data demonstrate differential susceptibility of the different adipose depots to the development of age-associated insulin resistance and inflammation.
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Rojas et al. (2015) studied this question.
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