title: Epigallocatechin gallate prevents inflammation by reducing macrophage infiltration and inhibiting tumor necrosis factor-α signaling in the pancreas of rats on a high-fat diet.
abstract: In this study, we hypothesized that epigallocatechin gallate (EGCG) would suppress inflammation in the pancreas, and thus, we investigated the effects that EGCG administration had in the pancreas of rats fed a high-fat diet (HFD). To test our hypothesis, 30 male Sprague-Dawley rats were divided into 2 groups: normal diet (control) group and HFD group. When there was a significant difference in body weight between the 2 groups (P < .05), the HFD group was further divided into 2 subgroups: the HFD group (HFD, n = 10, 16 weeks) and the EGCG group (HFD + 3.2 g/kg EGCG, n = 10, 16 weeks). Metabolite levels and the expression of inflammatory markers (tumor necrosis factor alpha [TNF-α], interleukin 6 [IL-6], and toll-like receptor 4) were measured using standard biochemical techniques. Insulin secretion and pancreatic histology were also evaluated. Epigallocatechin gallate significantly decreased fasting insulin levels as well as the homeostasis model assessment-insulin resistance index. In the HFD group, the average glucose infusion rate and the TNF-α and IL-6 levels increased, whereas toll-like receptor 4 and TNF receptor-associated factor-6 did not. A pathologic analysis of pancreatic tissue revealed an increase in inflammatory TNF-α and infiltrating CD68+ macrophages in the islets of the HFD rats, but rarely is this observed in the in the HFD + EGCG rats. Overall, these data suggest that EGCG suppresses inflammation, partially reverses metabolic abnormalities, and ultimately increases insulin sensitivity in the pancreas of HFD rats.
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China. Electronic address: vanilla421@163.com.
authors.forename: Yanli
authors.initials: Y
authors.lastname: Cao
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Suqing
authors.initials: S
authors.lastname: Bao
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Wanli
authors.initials: W
authors.lastname: Yang
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Jin
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Zhongyan
authors.initials: Z
authors.lastname: Shan
authors.affiliation: Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, First Affiliated Hospital of China Medical University, Shenyang, 110001, PR China.
authors.forename: Weiping
authors.initials: W
authors.lastname: Teng
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D016207:Cytokines / Q000097:blood; D059305:Diet, High-Fat / Q000009:adverse effects*; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000187:drug effects / Q000473:pathology; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D010179:Pancreas / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001786:Blood Glucose; D002392:Catechin; D016207:Cytokines; D018836:Inflammation Mediators; D007328:Insulin; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C045651:epigallocatechin gallate
keywords: Epigallocatechin gallate; Inflammation; Obesity; Pancreas; Rat