title: Dietary polyherbal supplementation decreases CD3+ cell infiltration into pancreatic islets and prevents hyperglycemia in nonobese diabetic mice.
abstract: Type 1 diabetes mellitus results from autoimmune-mediated destruction of pancreatic islet β-cells, a process associated with inflammatory signals. We hypothesized that dietary supplementation with botanicals known to contain anti-inflammatory properties would prevent losses in functional β-cell mass in nonobese diabetic (NOD) mice, a rodent model of autoimmune-mediated islet inflammation that spontaneously develops diabetes. Female NOD mice, a model of spontaneous autoimmune diabetes, were fed a diet supplemented with herbal extracts (1.916 g total botanical extracts per 1 kg of diet) over a 12-week period. The mice consumed isocaloric matched diets without (controls) and with polyherbal supplementation (PHS) ad libitum starting at a prediabetic stage (age 6 weeks) for 12 weeks. Control mice developed hyperglycemia (>180 mg/dL) within 16 weeks (n = 9). By contrast, mice receiving the PHS diet did not develop hyperglycemia by 18 weeks (n = 8). Insulin-positive cell mass within pancreatic islets was 31.9% greater in PHS mice relative to controls. We also detected a 26% decrease in CD3(+) lymphocytic infiltration in PHS mice relative to mice consuming a control diet. In vitro assays revealed reduced β-cell expression of the chemokines CCL2 and CXCL10 after overnight PHS addition to the culture media. We conclude that dietary PHS delays initiation of autoimmune-mediated β-cell destruction and subsequent onset of diabetes mellitus by diminishing islet inflammatory responses.
authors: Department of Nutrition, University of Tennessee, Knoxville, TN, USA.
authors: Susan J
authors: SJ
authors: Burke
authors: Department of Nutrition, University of Tennessee, Knoxville, TN, USA; Department of Surgery, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN, USA.
authors: Michael D
authors: MD
authors: Karlstad
authors: Department of Surgery, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN, USA.
authors: Caroline P
authors: CP
authors: Conley
authors: Department of Biomedical and Diagnostic Sciences, University of Tennessee, College of Veterinary Medicine, Knoxville, TN, USA.
authors: Danielle
authors: D
authors: Reel
authors: Department of Nutrition, University of Tennessee, Knoxville, TN, USA.
authors: Jay
authors: J
authors: Whelan
authors: Department of Nutrition, University of Tennessee, Knoxville, TN, USA; Department of Surgery, Graduate School of Medicine, University of Tennessee Medical Center, Knoxville, TN, USA. Electronic address: Jason.collier@pbrc.edu.
authors: J Jason
authors: JJ
authors: Collier
mesh_terms: D000818:Animals; D002460:Cell Line; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D054357:Chemokine CXCL10 / Q000235:genetics / Q000378:metabolism; D004032:Diet / Q000662:veterinary; D019587:Dietary Supplements; D005260:Female; D006943:Hyperglycemia / Q000188:drug therapy*; D018836:Inflammation Mediators / Q000494:pharmacology; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D016688:Mice, Inbred NOD; D010936:Plant Extracts / Q000494:pharmacology*; D011236:Prediabetic State / Q000188:drug therapy; D051381:Rats
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D054357:Chemokine CXCL10; C485433:Cxcl10 protein, mouse; D018836:Inflammation Mediators; D010936:Plant Extracts
keywords: Autoimmunity; Chemokine; Diabetes; Inflammation; Nonobese diabetic mouse