Influence of gender and time diet exposure on endocrine pancreas remodeling in response to high fat diet-induced metabolic disturbances in mice

Oliveira, Ricardo B.; Maschio, Daniela A.; Carvalho, Carolina P. F.; Collares-Buzato, Carla Beatriz

doi:10.1016/j.aanat.2015.01.007

Cited by 34 publications

(45 citation statements)

References 46 publications

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“…[15][16][17][18][19] To investigate whether supplementation with sodium butyrate has also an effect on insulin secretion, batches of isolated pancreatic islets from mice of all experimental groups were in vitro exposed to 2.8 mM or 16.7 mM glucose for 60 min (Figure 2). At basal condition (2.8 mM glucose), islets isolated from mice of the HF group showed a significant increase in basal insulin release as compared to control group (Figure 2(a)), which is in agreement with our previous data.…”

Section: Resultsmentioning

confidence: 99%

“…39 It is well known that the pancreatic beta cell plays a central role in the T2DM pathogenesis, displaying an adaptive response in order to compensate the resistance of peripheral tissues to insulin. 5,[16][17][18][19] For that, beta cells initially enhance the biosynthesis and release of this hormone followed by an increment of beta-cell mass by hypertrophy and/or hyperplasia. When the beta cells fail to maintain the normoglycemia, T2DM is triggered, resulting in insulin secretory impairment and then beta-cell death by apoptosis at advanced stages, which leads to an irreversible body dependence on exogenous insulin.…”

Section: Discussionmentioning

confidence: 99%

“…These procedures were performed as previously described 19,40,41 and at the same period during the day (9 a.m.-11 a.m.). The blood glucose concentration was measured using an Accu-Chek Advantage II glucometer (Roche Diagnostic, Switzerland).…”

Section: Weight Gain and Metabolic Evaluationmentioning

confidence: 99%

“…the typical arrangement of beta-and non-beta-cells within the islet), 42 the pancreas sections were processed for dual immunofluorescence for insulin (using the anti-insulin, cat number A0564, Dako, USA) and glucagon (using the antiglucagon, cat number A0565, Dako, USA) using a standard protocol 19,40 and observed by confocal laser microscopy (LSM 510-Zeiss, Germany).…”

Section: Pancreas and Liver Histology And Morphometrymentioning

confidence: 99%

“…[15][16][17][18] At initial stages, beta cells increase insulin biosynthesis and release but, subsequently, due to the continuous resistance of biological tissues to insulin, beta cell mass expands to promote a further increase in secretion of this hormone necessary for the maintenance of normoglycemia. 15,[17][18][19] In advanced stages, the constant demand for insulin hypersecretion in association with long-term exposition to hyperglycemia/dyslipidemia and a chronic inflammatory state within the pancreatic islet milieu result in secretory impairment and then beta-cell death by apoptosis, reducing its mass in the pancreas. 5,[15][16][17]20,21 As a consequence, replacement therapy with insulin is needed to recover glucose homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

Matheus

Monteiro

Oliveira

et al. 2017

Exp Biol Med (Maywood)

107

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Butyrate is a short-chain fatty acid produced by the intestinal microbiota through the fermentation of non-absorbable carbohydrates and proteins (e.g. fibers). Sodium butyrate incorporated into the diet displayed a protective action on metabolic, hepatic, pancreatic and intestinal alterations induced by high-fat diet in mice, resulting in significant inhibition of the development of a prediabetic state. Thus, our data suggest that butyrate may have a potential therapeutic use in the treatment of type 2 diabetes and related disorders. AbstractIn this study, we investigated the effect of diet supplementation with sodium butyrate (5% w/w), a short-chain fatty acid produced by the intestinal microbiota, on metabolic parameters, body adiposity, hepatic and pancreatic lipid accumulation, beta cell function/mass as well as on the structure and function of the tight junction-mediated intestinal epithelial barrier in both normal and obese/prediabetic C57 mice fed a regular (control) or high-fat diet for 60 days, respectively. Butyrate treatment significantly inhibited all the high-fat-induced metabolic dysfunctions evaluated, i.e. significantly reduced the weight gain and body adiposity as well as the insulin resistant state, hyperglycemia and hyperinsulinemia, without changing food intake. In addition, high-fat-fed mice treated with this short-chain fatty acid displayed no compensatory hyperplasia of pancreatic beta cells nor marked hepatic steatosis as seen in prediabetic mice after high-fat diet only. Isolated pancreatic islets from high-fat-fed mice treated with butyrate showed improvement of the insulin secretion, which was associated with a significant decrease in lipid accumulation within the pancreas. Butyrate enhanced the intestinal epithelial barrier, as revealed by the FITC-Dextran permeability assay, which was accompanied by a significant increase in the junctional content of the tight junction-associated claudin-1 in intestinal epithelia of jejunum, ileum, and colon of both control and high-fat mice. In conclusion, our results showed that diet supplementation with butyrate inhibits the deleterious effects of high-fat diet intake on metabolic parameters and structure/function of several tissues/ organs associated with type 2 diabetes mellitus in a mouse model, suggesting a potential use of this short-chain fatty acid in the treatment of this endocrine-metabolic disorder.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Weight Gain and Metabolic Evaluationmentioning

confidence: 99%

Section: Pancreas and Liver Histology And Morphometrymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

Matheus

Monteiro

Oliveira

et al. 2017

Exp Biol Med (Maywood)

107

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Methylation of Tcf712 promoter by high‐fat diet impairs β‐cell function in mouse pancreatic islets

Shi

et al. 2018

Diabetes Metabolism Res

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Islet cells are the source of Wnts that can induce beta‐cell proliferation in vitro

Maschio

Matheus

Collares-Buzato

2019

Journal Cellular Physiology

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Wnt proteins act mainly as paracrine signals regulating cell proliferation and differentiation. The canonical Wnt pathway has recently been associated with pancreas development and the onset of type 2 diabetes in rodent and human but the underlying mechanisms are still unclear. The aim of this work was threefold: (a) to screen for Wnt expressed by murine pancreas/islet cells, (b) to investigate whether the Wnt gene expression profile can be changed in hyperplastic islets from type 2 prediabetic mice (fed a high-fat diet), and (c) to verify whether soluble factors (namely Wnts) released by pancreatic islets affect insulin secretion and proliferation of a betacell line in vitro condition. The majority of the Wnt subtypes are expressed by islet cells, such as Wnts 2, 2b, 3, 3a, 4, 5a, 5b, 6, 7a, 7b, 8a, 8b, 9a, 9b, and 11, while in the whole pancreas homogenates were found the same subtypes, except Wnts 3, 6, 7a, and 7b. Among all the Wnts, the Wnts 3a and 5b showed a significantly increased gene expression in hyperplastic islets from prediabetic mice compared with those from control mice. Furthermore, we observed that coculture with hyperplastic or nonhyperplastic islets did not change the secretory function of the mouse insulinoma clone 6 (MIN6) beta cells but induced a significant increase in cell proliferation in this lineage, which was partially blocked by the IWR-1 and IWP-2 Wnt inhibitors. In conclusion, we demonstrated that murine pancreas/islet cells can secrete Wnts, and that islet-released Wnts may participate in the regulation of beta-cell mass under normal and prediabetic conditions.

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Influence of gender and time diet exposure on endocrine pancreas remodeling in response to high fat diet-induced metabolic disturbances in mice

Cited by 34 publications

References 46 publications

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

Butyrate reduces high-fat diet-induced metabolic alterations, hepatic steatosis and pancreatic beta cell and intestinal barrier dysfunctions in prediabetic mice

Methylation of Tcf712 promoter by high‐fat diet impairs β‐cell function in mouse pancreatic islets

Islet cells are the source of Wnts that can induce beta‐cell proliferation in vitro

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