Supplementation with anthocyanidins (AC), i.e. cyanidin and delphinidin, caused a decrease in body weight gain and fat deposits in mice fed a high fat diet (HF). This study investigated the capacity of dietary AC to promote “beiging” of subcutaneous white adipose tissue (sWAT), through increased mitochondrial biogenesis and thermogenesis. C57BL/6J male mice were fed control (C) or HF diets, with or without supplementation with 40 mg AC/kg body weight (CA and HFA). After 15 w, HF consumption caused obesity and increased eWAT weight, which were mitigated by AC supplementation. Adipocyte diameter was higher in HF than in C, CA and HFA mice. H&E stain showed images compatible with beiging in both AC-treated groups. Electron microscopy (TEM) showed a fewer number of mitochondria in HF but not in HFA mice. TEM findings were confirmed by measuring the expression of mitochondrial protein markers. AC prevented HF-induced inhibition of the pathway leading to mitochondria biogenesis (PPARγ, PRDM16, PGC-1α), and thermogenic respiration (UCP-1). Mice consuming the control diet plus AC also showed upregulation of PPARγ, PRDM16, PGC-1α. Findings suggest that consumption of selct AC could be an important strategy to mitigate HF-induced obesity in part via activation of adipocyte mitochondriogenesis and beiging.
Anthocyanidins promotes beiging of white adipose tissue in mice fed a high fat diet / C.M. Rodriguez-Lanzi, E. Cremonini, M. Marino, D. Iglesias, A. Mastaloudis, S. Wood, S. Hester, C.G. Fraga, A.P.I. Oteiza. ((Intervento presentato al convegno Redox homeostasis: from signaling to damage tenutosi a Ferrara nel 2019.
Anthocyanidins promotes beiging of white adipose tissue in mice fed a high fat diet
M. MarinoSecondo
;
2019
Abstract
Supplementation with anthocyanidins (AC), i.e. cyanidin and delphinidin, caused a decrease in body weight gain and fat deposits in mice fed a high fat diet (HF). This study investigated the capacity of dietary AC to promote “beiging” of subcutaneous white adipose tissue (sWAT), through increased mitochondrial biogenesis and thermogenesis. C57BL/6J male mice were fed control (C) or HF diets, with or without supplementation with 40 mg AC/kg body weight (CA and HFA). After 15 w, HF consumption caused obesity and increased eWAT weight, which were mitigated by AC supplementation. Adipocyte diameter was higher in HF than in C, CA and HFA mice. H&E stain showed images compatible with beiging in both AC-treated groups. Electron microscopy (TEM) showed a fewer number of mitochondria in HF but not in HFA mice. TEM findings were confirmed by measuring the expression of mitochondrial protein markers. AC prevented HF-induced inhibition of the pathway leading to mitochondria biogenesis (PPARγ, PRDM16, PGC-1α), and thermogenic respiration (UCP-1). Mice consuming the control diet plus AC also showed upregulation of PPARγ, PRDM16, PGC-1α. Findings suggest that consumption of selct AC could be an important strategy to mitigate HF-induced obesity in part via activation of adipocyte mitochondriogenesis and beiging.File | Dimensione | Formato | |
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