Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice

Leite, Nayara C.; Paula, Flavia; Borck, Patrícia Cristine; Vettorazzi, Jean Franciesco; Branco, Renato Chaves Souto; Lubaczeuski, Camila; Boschero, Antônio Carlos; Zoppi, Cláudio C.; Carneiro, Everardo M.

doi:10.1038/srep33464

Cited by 15 publications

(22 citation statements)

References 42 publications

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“…In 2006 our research group observed the absence of amplifying pathways in islets from MSG‐obese rats, which was also found in the present study. However, previous study has demonstrated that insulin secretion induced by amplifying pathway is not altered in pancreatic islets from obese mice on a high‐fat diet . Thus, further studies will be necessary in order to better understand which mechanisms are underlying this difference between different animals model of obesity.…”

Section: Discussionmentioning

confidence: 95%

“…However, previous study has demonstrated that insulin secretion induced by amplifying pathway is not altered in pancreatic islets from obese mice on a high-fat diet. 43 Thus, further studies will be necessary in order to better understand which mechanisms are underlying this difference between different animals model of obesity. Our data show that chronic exercise training reduces GSIS by inhibiting amplifying pathways in pancreatic islets; an effect that was more evident in islets from MSG-EXE rats.…”

Section: Discussionmentioning

confidence: 99%

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Swimming training reduces glucose‐amplifying pathway and cholinergic responses in islets from lean‐ and MSG‐obese rats

Borck

Leite

Valcanaia

et al. 2019

Clin Exp Pharma Physio

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Here, we investigate the effects of exercise training on glucose‐ and cholinergic‐induced insulin secretion in pancreatic islets from obese and lean rats. Male Wistar rats were treated with monosodium glutamate (MSG) for the first 5 days of life, while control (CON) rats received saline. At 21 days, the rats were divided into exercised (EXE) and sedentary (SED) groups. The EXE rats swam for 30 minutes, three times/week, for 10 weeks. After this, MSG‐SED rats showed hyperglycaemia, hypertriglyceridaemia and hyperinsulinaemia. Besides, islets from MSG‐SED rats exhibited increased glucose‐stimulated insulin secretion (GSIS), followed by impaired glucose sensitivity, absence of glucose‐amplifying pathway and weak cholinergic response. In contrast, adiposity, hyperinsulinaemia and hypertriglyceridaemia were reduced in MSG‐EXE rats. Moreover, islets from MSG‐EXE rats exhibited lower GSIS and improved islet glucose sensitivity, without restoration of the glucose‐amplifying pathway or alteration in the weak cholinergic effect of these islets. In islets from CON‐EXE rats we also observed reduced GSIS and absence of glucose‐amplifying effects and an accentuated reduction in cholinergic insulinotropic responses, without effect on glucose sensitivity in pancreatic islets from this group. Neither obesity nor exercise modified Muscarinic Receptor 3 (M3R) immunocontent or its downstream pathways (PKC and PKA). Moreover, only CON‐EXE showed increased GSIS in the presence of calcium blocker, Thapsigargin. In conclusion, swimming training reduces GSIS and cholinergic responsiveness in isolated pancreatic islets from lean and hypothalamic obese rats, which could be due to the inhibition of glucose‐amplifying pathways.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Swimming training reduces glucose‐amplifying pathway and cholinergic responses in islets from lean‐ and MSG‐obese rats

Borck

Leite

Valcanaia

et al. 2019

Clin Exp Pharma Physio

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“…However, other mechanisms may be underlying the outcome induced by HFD on GSIS in protein‐restricted mice. In this sense, we have recently shown that the increment on GSIS in RH pancreatic islets is modulated by mitochondrial‐amplifying pathways of insulin secretion (51). Pancreatic islets from RH mice displayed lower mitochondrial membrane potential and increased ROS generation but without differences in ATP levels.…”

Section: Discussionmentioning

confidence: 99%

Protein malnutrition blunts the increment of taurine transporter expression by a high‐fat diet and impairs taurine reestablishment of insulin secretion

et al. 2017

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Taurine (Tau) restores β-cell function in obesity; however, its action is lost in malnourished obese rodents. Here, we investigated the mechanisms involved in the lack of effects of Tau in this model. C57BL/6 mice were fed a control diet (CD) (14% protein) or a protein-restricted diet (RD) (6% protein) for 6 wk. Afterward, mice received a high-fat diet (HFD) for 8 wk [CD + HFD (CH) and RD + HFD (RH)] with or without 5% Tau supplementation after weaning on their drinking water [CH + Tau (CHT) and RH + Tau (RHT)]. The HFD increased insulin secretion through mitochondrial metabolism in CH and RH. Tau prevented all those alterations in CHT only. The expression of the taurine transporter (Tau-T), as well as Tau content in pancreatic islets, was increased in CH but had no effect on RH. Protein malnutrition programs β cells and impairs Tau-induced restoration of mitochondrial metabolism and biogenesis. This may be associated with modulation of the expression of Tau-T in pancreatic islets, which may be responsible for the absence of effect of Tau in protein-malnourished obese mice.-Branco, R. C. S., Camargo, R. L., Batista, T. M., Vettorazzi, J. F., Borck, P. C., dos Santos-Silva, J. C. R., Boschero, A. C., Zoppi, C. C., Carneiro, E. M. Protein malnutrition blunts the increment of taurine transporter expression by a high-fat diet and impairs taurine reestablishment of insulin secretion.

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“…It is known that diet-induced obesity, in mice, also provokes glucose intolerance accompanied by increased insulin secretion, which compensates for the peripheral insulin resistance [ 17 ]. This phenomenon has also been detected in metabolic programmed mice fed on a low-protein diet in early life followed by regular diet [ 2 ] or high-fat diet [ 5 , 18 ] during adulthood. Here, we confirmed these results with the LP + HF showing impaired insulin sensitivity and glucose tolerance, as well as an increased insulin secretion.…”

Section: Discussionmentioning

confidence: 87%

“…We have shown that mice fed on a low-protein diet in adolescence, followed by a high-fat diet during adulthood, develop glucose intolerance, insulin resistance, and reduced insulin secretion, compared to those fed on a high-fat diet during the whole experimental period [ 5 ]. This indicates that the metabolic programming, induced by malnutrition in early life, impairs insulin-glucose homeostasis to a greater extent than obesity per se.…”

Section: Introductionmentioning

confidence: 99%

Vagotomy Reduces Insulin Clearance in Obese Mice Programmed by Low-Protein Diet in the Adolescence

et al. 2017

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The aim of this study was to investigate the effect of subdiaphragmatic vagotomy on insulin sensitivity, secretion, and degradation in metabolic programmed mice, induced by a low-protein diet early in life, followed by exposure to a high-fat diet in adulthood. Weaned 30-day-old C57Bl/6 mice were submitted to a low-protein diet (6% protein). After 4 weeks, the mice were distributed into three groups: LP group, which continued receiving a low-protein diet; LP + HF group, which started to receive a high-fat diet; and LP + HFvag group, which underwent vagotomy and also was kept at a high-fat diet. Glucose-stimulated insulin secretion (GSIS) in isolated islets, ipGTT, ipITT, in vivo insulin clearance, and liver expression of the insulin-degrading enzyme (IDE) was accessed. Vagotomy improved glucose tolerance and reduced insulin secretion but did not alter adiposity and insulin sensitivity in the LP + HFvag, compared with the LP + HF group. Improvement in glucose tolerance was accompanied by increased insulinemia, probably due to a diminished insulin clearance, as judged by the lower C-peptide : insulin ratio, during the ipGTT. Finally, vagotomy also reduced liver IDE expression in this group. In conclusion, when submitted to vagotomy, the metabolic programmed mice showed improved glucose tolerance, associated with an increase of plasma insulin concentration as a result of insulin clearance reduction, a phenomenon probably due to diminished liver IDE expression.

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Protein malnutrition potentiates the amplifying pathway of insulin secretion in adult obese mice

Cited by 15 publications

References 42 publications

Swimming training reduces glucose‐amplifying pathway and cholinergic responses in islets from lean‐ and MSG‐obese rats

Swimming training reduces glucose‐amplifying pathway and cholinergic responses in islets from lean‐ and MSG‐obese rats

Protein malnutrition blunts the increment of taurine transporter expression by a high‐fat diet and impairs taurine reestablishment of insulin secretion

Vagotomy Reduces Insulin Clearance in Obese Mice Programmed by Low-Protein Diet in the Adolescence

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