Abstract
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.
Highlights
Obesity has reached epidemic proportions in both developed and developing countries; concurrently, the incidences of metabolic syndrome and type 2 diabetes are increasing rapidly [1]
While elevated pro-inflammatory macrophages were detected in epididymal fat of both High fructose corn syrup (HFCS)- and SUC-fed mice, reduced anti-inflammatory macrophages were detected in HFCS-fed mice but not SUC-fed mice. These results indicate that more severe adipose inflammation is induced by HFCS compared to SUC, which is in line with the exacerbated insulin resistant state exhibited by HFCS-feeding
The recruitment of pro-inflammatory macrophages in intra-abdominal fat is promoted by both HFCS and SUC, inducing adipose inflammation, which subsequently leads to deleterious effects on insulin sensitivity
Summary
Obesity has reached epidemic proportions in both developed and developing countries; concurrently, the incidences of metabolic syndrome and type 2 diabetes are increasing rapidly [1]. It has been suggested that fructose-sweetened beverage consumption increases visceral adiposity and insulin resistance more severely than sucrose-sweetened beverage consumption [3]. The replacement of sucrose with HFCS is considered to have a major role in the pathogenesis of obesity and diabetes [6]. Studies have linked increased consumption of drinks containing either HFCS or fructose to obesity and/or insulin resistance [3,6,7,8,9]. One study reported that postprandial triglycerides were elevated by consumption of all fructose-containing beverages (HFCS, sucrose or fructose alone) compared to the glucose-containing beverages [9], suggesting that fructose, regardless of its form, promotes obesity. In-depth studies of the effects of the two most common sweeteners of HFCS and sucrose on adiposity, inflammation and insulin sensitivity are urgently needed
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
