Supplementing dietary sugar promotes endoplasmic reticulum stress-independent insulin resistance and fatty liver in goose

• Published in: Biochemical and biophysical research communications Vol. 476; no. 4; pp. 665 - 669
• Main Authors: Geng, Tuoyu, Zhao, Xing, Xia, Lili, Liu, Long, Li, Fuyuan, Yang, Biao, Wang, Qianqian, Montgomery, Sean, Cui, Hengmi, Gong, Daoqing
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 05.08.2016
• Subjects: abdominal fat; Animals; blood glucose; body weight; Cells, Cultured; corn; Diet; Dietary Carbohydrates - administration & dosage; Dietary Carbohydrates - adverse effects; endoplasmic reticulum; Endoplasmic reticulum stress; Endoplasmic Reticulum Stress - drug effects; Endoplasmic Reticulum Stress - physiology; ERS; fatty liver; Fatty Liver - etiology; Fatty Liver - metabolism; Fatty Liver - pathology; foodways; Geese; Gene Expression - drug effects; glucose; Glucose - administration & dosage; Glucose - adverse effects; glucose tolerance; Glucose Tolerance Test; Goose; GTT; Heat-Shock Proteins - genetics; hepatocytes; Hepatocytes - drug effects; Hepatocytes - metabolism; in vivo studies; Insulin resistance; Insulin Resistance - physiology; liver; mammals; NAFLD; Non-alcoholic fatty liver disease; oleic acid; Oleic Acid - administration & dosage; Organ Size - drug effects; overfeeding; palmitates; Palmitic Acid - administration & dosage; Palmitic Acid - adverse effects; NAFLD; Diet; Goose; GTT; ERS; Insulin resistance; IR; Glucose tolerance test; Non-alcoholic fatty liver disease; Endoplasmic reticulum stress
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2016.05.149

It is known that endoplasmic reticulum stress (ERS) contributes to insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) in mammals. However, we recently demonstrated that overfeeding with a traditional diet (mainly consisting of cooked maize) does not induce ERS in goose. As cellular studies show that high glucose and palmitate can trigger ERS in mammalian cells, we hypothesized that supplementing sugar to the traditional diet could induce ERS, thus promoting insulin resistance and fatty liver. To test the hypothesis, we first treated goose primary hepatocytes with high glucose (25 mM and 50 mM) and palmitate (0.5 mM) supplemented with or without 0.25 mM oleate. Data indicated that, as in mammalian cells, high glucose and palmitate indeed induced ERS in goose primary hepatocytes, and palmitate-induced ERS was suppressed by supplemental 0.25 mM oleate. We then tested the hypothesis with an in vivo study, in which Landes geese overfed with traditional or novel diets (i.e., the traditional diet supplemented with sugar) were compared with control geese (normally fed with cooked maize) for ERS, IR and fatty liver. The differences in glucose tolerance, insulin tolerance and postprandial blood glucose between the geese overfed with traditional and novel diets suggested that supplementing dietary sugar promoted IR. This promotion was accompanied with an increasing trend of liver weight and abdominal fat weight relative to body weight. Surprisingly, compared to overfeeding with the traditional diet, overfeeding with the novel diet did not induce ERS, even further suppressed ERS in goose fatty liver. Together, our findings suggest that supplementing dietary sugar promotes ERS-independent IR and fatty liver in goose. It is intriguing to discover the factor(s) protecting goose liver from ERS as well as the non-ERS mechanism underlying IR. •Supplementing dietary sugar promotes ERS-independent IR and fatty liver in goose.•Protective components against hepatic ERS are inside and outside goose hepatocytes.•High glucose and palmitate promote ERS in goose hepatocytes.•Palmitate induced ERS is blocked by supplemental oleate in goose hepatocytes.