Abstract
Holothurian glycosaminoglycan isolated from Apostichopus japonicus (named AHG) can suppress hepatic glucose production in insulin resistant hepatocytes, but its effects on glucose metabolism in vivo are unknown. The present study was conducted to investigate the effects of AHG on hyperglycemia in the liver of insulin resistant mice induced by a high-fat diet (HFD) for 12 weeks. The results demonstrated that AHG supplementation apparently reduced body weight, blood glucose level, and serum insulin content in a dose-dependent manner in HFD-fed mice. The protein levels and gene expression of gluconeogenesis rate-limiting enzymes G6Pase and PEPCK were remarkedly suppressed in the insulin resistant liver. In addition, although the total expression of IRS1, Akt, and AMPK in the insulin resistant liver was not affected by AHG supplementation, the phosphorylation of IRS1, Akt, and AMPK were clearly elevated by AHG treatment. These results suggest that AHG could be a promising natural marine product for the development of an antihyperglycemic agent.
Highlights
Type 2 diabetes mellitus(T2DM) is characterized by long-term persistent hyperglycemia with several complications such as eye injury, renal failure, cardiovascular disease, and nervous system damage [1]
We investigated the protective ability of AHG on dysregulated glucose homeostasis in insulin resistant mice induced by a high-fat diet (HFD)
AHG was shown to have a therapeutic effect on hepatic glucose metabolism in vitro, there is no report target the effect of AHG on glucose metabolism in vivo
Summary
Type 2 diabetes mellitus(T2DM) is characterized by long-term persistent hyperglycemia with several complications such as eye injury, renal failure, cardiovascular disease, and nervous system damage [1]. T2DM has become a chronic disease globally. Insulin resistance is the hallmark of T2DM and describes a condition whereby the ability of insulin to trigger glucose uptake, metabolism, or storage is impaired [3,4]. As the major site of glucose utilization during the post-prandial period and the main human tissue of glucose synthetization, the liver is the vital target organ of insulin resistance, and liver insulin resistance is the main reason for the development of T2DM [5,6]. When insulin resistance develops in the liver, increased hepatic glucose production and decreased glucose utilization contribute to the elevated level of blood glucose [7]
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