Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Singh, Himadri; Ganneru, Sireesha; Malakapalli, Venkata; Chalasani, Maniprabha; Nappanveettil, Giridharan; Bhonde, Ramesh; Venkatesan, Vijayalakshmi

doi:10.1080/19382014.2014.998099

Cited by 16 publications

(18 citation statements)

References 63 publications

(87 reference statements)

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“…The result showed that the levels of FINS were significantly increased in the CP group at the late stage of CP induction. Additionally, the elevated levels were similar to those reported in other studies in rats with hyperinsulinemia, 40,41 indicating that hyperinsulinemia in rats in the CP group was successfully induced. We also measured the changes in FBG levels in rats.…”

Section: Discussionsupporting

confidence: 88%

Chronic periodontitis induces the proliferation of pancreatic β‐cells to cause hyperinsulinemia in a rat model

Ye,

Lv,

et al. 2023

J of Periodontal Research

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Background and ObjectiveThe purpose of this study was to determine if chronic periodontitis (CP) may induce hyperinsulinemia and may have the effect of on pancreatic β‐cell proliferation in a rat model.Materials and MethodsTwelve male Sprague–Dawley rats were divided into two groups: the CP group and the control group (Con group). The following contents were evaluated: pathological changes in periodontal soft and hard tissues; serum lipopolysaccharide (LPS) level, serum fasting insulin (FINS) level, fasting blood glucose (FBG) level, and homeostasis model assessment (HOMA) β (HOMA‐β) index; histopathological examination of islets; immunohistochemistry of insulin and p‐Smad2 expression in islets; immunofluorescence of changes in the relative number of β‐cells and the number of Ki67‐positive β‐cells. Western blotting was used to analyze p‐Smad2/Smad2 levels. Results were analyzed by two independent samples t tests.ResultsIncreased serum LPS level, FINS level, and HOMA‐β index were observed in the rats of the CP group; FBG level did not change significantly; histological assessments showed an enlarged islet area, increased insulin content, relatively increased β‐cells, increased Ki67‐positive β‐cells, and decreased p‐Smad2 expression in islets in the rats of the CP group.ConclusionOur study results link CP‐induced hyperinsulinemia with changes in islets, such as islet hyperplasia and compensatory β‐cell proliferation, by using a CP rat model.

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Section: Discussionsupporting

confidence: 88%

Chronic periodontitis induces the proliferation of pancreatic β‐cells to cause hyperinsulinemia in a rat model

Ye,

Lv,

et al. 2023

J of Periodontal Research

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“…Counterintuitively, we observed the presence of hyperinsulinaemia and enhanced in vivo insulin secretion response in SFA-HFD-fed mice despite β-cell dedifferentiation and reduced ex vivo islet insulin secretion; however, this may be explained by coincident inflammation. Indeed, genetic or diet-induced models of obesity contribute to both hyperinsulinaemia and pancreatic inflammation (31)(32)(33)(34)(35)(36) . Through various mechanisms, including increased fibrosis (32) or elevated islet blood perfusion (32,37) , inflammation in the pancreas can contribute to hyperinsulinaemia and downstream tissue dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Dietary substitution of SFA with MUFA within high-fat diets attenuates hyperinsulinaemia and pancreatic islet dysfunction

et al. 2020

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Preliminary evidence has suggested that high-fat diets (HFD) enriched with SFA, but not MUFA, promote hyperinsulinaemia and pancreatic hypertrophy with insulin resistance. The objective of this study was to determine whether the substitution of dietary MUFA within a HFD could attenuate the progression of pancreatic islet dysfunction seen with prolonged SFA-HFD. For 32 weeks, C57BL/6J mice were fed either: (1) low-fat diet, (2) SFA-HFD or (3) SFA-HFD for 16 weeks, then switched to MUFA-HFD for 16 weeks (SFA-to-MUFA-HFD). Fasting insulin was assessed throughout the study; islets were isolated following the intervention. Substituting SFA with MUFA-HFD prevented the progression of hyperinsulinaemia observed in SFA-HFD mice (P < 0·001). Glucose-stimulated insulin secretion from isolated islets was reduced by SFA-HFD, yet not fully affected by SFA-to-MUFA-HFD. Markers of β-cell identity (Ins2, Nkx6.1, Ngn3, Rfx6, Pdx1 and Pax6) were reduced, and islet inflammation was increased (IL-1β, 3·0-fold, P = 0·007; CD68, 2·9-fold, P = 0·001; Il-6, 1·1-fold, P = 0·437) in SFA-HFD – effects not seen with SFA-to-MUFA-HFD. Switching to MUFA-HFD can partly attenuate the progression of SFA-HFD-induced hyperinsulinaemia, pancreatic inflammation and impairments in β-cell function. While further work is required from a mechanistic perspective, dietary fat may mediate its effect in an IL-1β–AMP-activated protein kinase α1-dependent fashion. Future work should assess the potential translation of the modulation of metabolic inflammation in man.

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“…10 From 35 days of age, these mutants portray noticeable spontaneous obesity and a kinky tail. 11 With age, an exponential increase in body weight accompanied by hyperphagia, polydipsia, polyuria, and glycosuria are observed in these rats. 12 They also portray altered biochemical and metabolic features like IR, IGT, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, hyperleptinaemia, and hypertension 11,12 with hypertrophy of the insulin-sensitive target organs.…”

Section: Introductionmentioning

confidence: 87%

“…11 With age, an exponential increase in body weight accompanied by hyperphagia, polydipsia, polyuria, and glycosuria are observed in these rats. 12 They also portray altered biochemical and metabolic features like IR, IGT, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, hyperleptinaemia, and hypertension 11,12 with hypertrophy of the insulin-sensitive target organs. They depict accelerated aging with a shortened life span of 1.5 years and display an array of secondary complications warranting their application(s) in biomedical research, more pertinent to the area of MetS.…”

Section: Introductionmentioning

confidence: 87%

Metabolic Syndrome Predisposes to Osteoarthritis: Lessons from Model System

Pragasam

Venkatesan

2020

CARTILAGE

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Objective The present study aims to assess for temporal changes in tibial subchondral bone and cartilage in WNIN/Gr-Ob rats (portraying obesity, insulin resistance, dyslipidemia, impaired glucose tolerance, hypertension) in comparison with Wistar controls (WNIN) using anthropometry, micro-computed tomography (micro-CT), scanning electron microscopy (SEM), histopathology, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence. Design Body weight, abdominal circumference, body mass index (BMI), lean/fat mass, serum tumor necrosis factor (TNF)-α levels were measured (ELISA), followed by ultrastructural analysis of tibial subchondral bone (micro-CT) and cartilage architecture (histopathology and SEM) in WNIN/Gr-Ob and WNIN rats with age (3, 6 and 9 months). Additionally, primary cultures of articular chondrocytes isolated from 6-month-old WNIN/Gr-Ob and WNIN rats were assessed for matrix metalloproteinase (MMP)-13 and Collagen type II (COL2A1) by immunofluorescence. Results WNIN/Gr-Ob rats exhibited frank obesity with increased BMI, lean and fat mass vis-à-vis significantly higher levels of serum TNF-α (6>9>3 months) as compared with the controls. With an increase in BMI, WNIN/Gr-Ob rats presented with tibial cartilage fibrillation, erosion, osteophyte formation (6 months) and subchondral bone cyst (9 months) confirmed by histology and SEM. An increase in subchondral trabecular bone volume (sclerosis with decreased plate porosity) was observed in all ages in WNIN/Gr-Ob rats compared to their Control. Gaining insights, primary cultures of articular chondrocytes complemented with altered cellular expressions of COL2A1 and MMP-13 from WNIN/Gr-Ob rats, indicating osteoarthritis (OA) progression. Conclusion Multiple metabolic perturbations featured in WNIN/Gr-Ob rats were effective to induce spontaneous OA-like degenerative changes affecting knee joints akin to human OA.

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Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Cited by 16 publications

References 63 publications

Chronic periodontitis induces the proliferation of pancreatic β‐cells to cause hyperinsulinemia in a rat model

Chronic periodontitis induces the proliferation of pancreatic β‐cells to cause hyperinsulinemia in a rat model

Dietary substitution of SFA with MUFA within high-fat diets attenuates hyperinsulinaemia and pancreatic islet dysfunction

Metabolic Syndrome Predisposes to Osteoarthritis: Lessons from Model System

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