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Oxidized Pork Induces Disorders of Glucose Metabolism in Mice
Author(s) -
Ge Yueting,
Li Bowen,
Yang Yuhui,
Feng Chuanxing,
Tang Xue,
Shi Yonghui,
Le Guowei,
Sun Jin
Publication year - 2021
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.202000859
Subject(s) - medicine , endocrinology , carbohydrate metabolism , glucose metabolism disorder , glycogen , glycolysis , insulin , gluconeogenesis , insulin receptor , glycogenolysis , metabolism , protein kinase b , oxidative stress , glucose uptake , biology , chemistry , insulin resistance , biochemistry , signal transduction
Scope Consumption of red meat, particularly processed red meat, has been reported to be associated with type 2 diabetes risk, and oxidized proteins and amino acids may be involved in this process. This study explores the effects of pork with varying degrees of oxidative injury caused by cooking on glucose metabolism in mice. Methods and results Cooked pork is freeze‐dried to prepare animal feed. Mice are fed either a control diet (CON), a low‐ (LOP), or a high‐oxidative injury pork diet (HOP) for 12 weeks. Intake of HOP causes hyperglycemia, hypoinsulinemia, and impaired glucose tolerance, indicating a glucose metabolism disorder. Accumulation of oxidation products increases oxidative stress and inflammatory response, which impairs pancreatic islet β cells function and reduces insulin secretion. Moreover, HOP‐mediated hyperglycemia can be partly attributed to elevated hepatic glucose output, as indicated by increased gluconeogenesis and glycogenolysis, and decreased glycolysis and glycogen content. Changes in these processes may be regulated by reduced insulin levels and suppression of the insulin receptor substrate‐1 (IRS‐1)/phosphoinositide 3‐kinase (PI3K)/protein kinase B (Akt) signaling pathway and its downstream signaling molecules. Conclusion HOP intake induces disorders of glucose metabolism by impairing pancreatic insulin secretion and increasing hepatic glucose output. Protein oxidation plays a key role in abnormal glucose metabolism induced by HOP.