Suppression of Ghrelin Exacerbates HFCS-Induced Adiposity and Insulin Resistance.
Suppression of Ghrelin Exacerbates HFCS-Induced Adiposity and Insulin Resistance.
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抑制生长素释放肽会加剧 HFCS 引起的肥胖和胰岛素抵抗
DOI:
10.3390/ijms18061302
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发表时间:
2017-06-19
影响因子:
5.6
通讯作者:
Sun Y
中科院分区:
文献类型:
--
作者:
Ma X;Lin L;Yue J;Wu CS;Guo CA;Wang R;Yu KJ;Devaraj S;Murano P;Chen Z;Sun Y
High fructose corn syrup (HFCS) is widely used as sweetener in processed foods and soft drinks in the United States, largely substituting sucrose (SUC). The orexigenic hormone ghrelin promotes obesity and insulin resistance; ghrelin responds differently to HFCS and SUC ingestion. Here we investigated the roles of ghrelin in HFCS- and SUC-induced adiposity and insulin resistance. To mimic soft drinks, 10-week-old male wild-type (WT) and ghrelin knockout (Ghrelin−/−) mice were subjected to ad lib. regular chow diet supplemented with either water (RD), 8% HFCS (HFCS), or 10% sucrose (SUC). We found that SUC-feeding induced more robust increases in body weight and body fat than HFCS-feeding. Comparing to SUC-fed mice, HFCS-fed mice showed lower body weight but higher circulating glucose and insulin levels. Interestingly, we also found that ghrelin deletion exacerbates HFCS-induced adiposity and inflammation in adipose tissues, as well as whole-body insulin resistance. Our findings suggest that HFCS and SUC have differential effects on lipid metabolism: while sucrose promotes obesogenesis, HFCS primarily enhances inflammation and insulin resistance, and ghrelin confers protective effects for these metabolic dysfunctions.