Why the study?
Brown adipose tissue acts as an endocrine organ, but the effects of salt loading and surgical removal of whitened interscapular brown adipose tissue on cardiac and adipose tissue pathology in metabolic syndrome remained unclear.
Does surgical removal of whitened interscapular brown adipose tissue ameliorate salt-induced cardiac pathology in a rat model of metabolic syndrome?
Does surgical removal of whitened interscapular brown adipose tissue ameliorate salt-induced cardiac pathology in a rat model of metabolic syndrome?
The conversion of interscapular brown adipose tissue to white adipose-like tissue contributes to salt-induced elevation of proinflammatory cytokines and exacerbation of cardiac pathology in a rat model of metabolic syndrome.
Implicates whitened BAT in salt-driven cardiac pathology; hypothesis-generating for adipose-targeted therapies in metabolic syndrome.
Brown adipose tissue (BAT) is an endocrine organ that contributes to thermogenesis and energy consumption. We investigated the effects of salt loading and surgical removal of whitened interscapular BAT (iBAT) on cardiac and adipose tissue pathology in DahlS.Z‐ Lepr fa / Lepr fa (DS/obese) rats, an animal model of metabolic syndrome (MetS). DS/obese rats were subjected to surgical removal of iBAT or sham surgery at 8 weeks of age and were provided with drinking water containing or not containing 0.3% NaCl for 4 weeks beginning at 9 weeks of age. Removal of iBAT suppressed the salt‐induced exacerbation of left ventricular inflammation, fibrosis, and diastolic dysfunction, but not that of hypertension development, in DS/obese rats. Salt loading attenuated adipocyte hypertrophy but enhanced inflammation in both visceral white adipose tissue (WAT) and iBAT. Although iBAT removal did not affect visceral WAT pathology in salt‐loaded DS/obese rats, it attenuated the elevation of circulating interleukin‐6 levels in these animals. Downregulation of uncoupling protein‐1 expression in iBAT of DS/obese rats was not affected by salt loading. Our results suggest that the conversion of iBAT to WAT‐like tissue contributes to a salt‐induced elevation of circulating proinflammatory cytokine levels that leads to exacerbation of cardiac pathology in this model of MetS.
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Komatsu et al. (2020) studied this question.
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