Insulin secretion and carbohydrate metabolism in experimental protein malnutrition

1980 ◽  
Vol 3 (3) ◽  
pp. 273-278 ◽  
Author(s):  
Romesh Khardori ◽  
J. S. Bajaj ◽  
M. G. Deo ◽  
D. D. Bansal
2017 ◽  
Vol 184 ◽  
pp. 86-93 ◽  
Author(s):  
Elisabeth Beythien ◽  
Manuela Wulf ◽  
Natascha Ille ◽  
Jörg Aurich ◽  
Christine Aurich

1975 ◽  
Vol 228 (4) ◽  
pp. 1046-1052 ◽  
Author(s):  
M Yajima ◽  
M Ui

Metabolic activities and their responses to catecholamines were studied in fasted rats exposed to simulated altitudes. Analysis of hepatic levels of gluconeogenic intermediates revealed the inhibition of gluconeogenesis between glyceric acid 3-P and fructose 6-P associated with a rise of the ratios of redox pairs such as lactate to pyruvate in livers of alkalotic rats. Inhibition of gluconeogenesis was indicated also by the suppressed incorporation of glutamate 14C into blood glucose. Since no activation was detected on glycolytic pathway of skeletal muscles, marked hyperlactacidemia during alkalosis appeared to result from the suppression of hepatic gluconeogenesis. Most of metabolic actions of epinephrine and isoproterenal known to be mediated via the beta receptor were significantly reduced but not completely abolished during alkalosis. Exceptionally, hyperinsulinemia induced by isoproterenol was completely reversed and replaced by hypoinsulinemia during alkalosis. Despite hypoinsulinemia, hyperglycemia induced by glucose load decreased more rapidly in alkalotic than in normal rats. In view of the fact that the adrenergic alpha receptor is involved in theinhibition of insulin secretion, the observed irregular modifications of catecholamine actions could be explained on the basis of a postulate that the adrenergic alpha-receptor functions are potentiated in alkalosis.


PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e30685 ◽  
Author(s):  
Renato Chaves Souto Branco ◽  
Júlio Cezar de Oliveira ◽  
Sabrina Grassiolli ◽  
Rosiane Aparecida Miranda ◽  
Luiz Felipe Barella ◽  
...  

2017 ◽  
Vol 50 ◽  
pp. 54-65 ◽  
Author(s):  
Patricia Cristine Borck ◽  
Thiago Martins Batista ◽  
Jean Franciesco Vettorazzi ◽  
Rafael Ludemann Camargo ◽  
Antonio Carlos Boschero ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Nayara Carvalho Leite ◽  
Flávia de Paula ◽  
Patrícia Cristine Borck ◽  
Jean Franciesco Vettorazzi ◽  
Renato Chaves Souto Branco ◽  
...  

1984 ◽  
Vol 16 (4) ◽  
pp. 239-246 ◽  
Author(s):  
ABIGAIL L. FOWDEN ◽  
R. S. COMLINE ◽  
MARIAN SILVER

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Daniele Mendes Guizoni ◽  
Israelle Netto Freitas ◽  
Jamaira Aparecida Victorio ◽  
Everardo Magalhaes Carneiro ◽  
Ana Paula Davel

Abstract Background: Pancreatic islets are highly vascularized and there is a correlation between endocrine pancreas function and pancreas perfusion. Protein malnutrition during early stages of development predispose to cardiovascular diseases, impaired insulin secretion and, type 2 diabetes. However, it is unknown if there are alterations in the pancreatic vasculature in response to malnutrition. Taurine (TAU) supplementation has been suggested as antihypertensive and improves endothelial function and insulin secretion in cardiometabolic disorders. Here, we investigated the effect of TAU in the vasorelaxation and endothelium-derived factors of the lieno-pancreatic artery from protein malnourished mice. Because lieno-pancreatic artery provides blood supply to pancreatic splenic lobe, a protective effect of TAU may result in cardiometabolic benefits. Methods: Post-weaned male C57Bl/6 mice fed a normal- (14%, NP) or a low-protein (6%, LP) diet for 90 days. Concomitantly, half of LP mice received 2.5% TAU in drinking water. Lieno-pancreatic artery (internal diameter ~ 160 µm) was isolated and concentration-response relaxation curves to acetylcholine (ACh), nitric oxide (NO)-donor (SNP), or hydrogen sulfide (H2S)-donor (NaHS) were performed. The involvement of NO and endothelium-derived hyperpolarization (EDH) in ACh-induced relaxation was assessed using L-NAME (NO synthase inhibitor) or KCl (to attenuate K+ efflux), respectively. Protein expression was evaluated by Western-blot; NO and H2S production by DAF-2A and WSP-1 fluorescence, respectively. Results: Endothelium-dependent relaxation to ACh was reduced in lieno-pancreatic artery from LP compared with NP group. Either KCl or L-NAME reduced ACh-induced relaxation, but only KCl abolished differences between LP and NP, suggesting that EDH rather than NO is involved in the impaired endothelium-dependent relaxation of LP. In accordance, relaxation to SNP, NO production, and endothelial NO synthase (eNOS) expression were not altered in lieno-pancreatic artery of LP group compared to NP. Because H2S has been demonstrated to have EDH activity in several blood vessels we investigated this pathway. H2S production and NaHS-induced relaxation were both reduced in lieno-pancreatic artery of LP group compared with NP. TAU treatment reversed the impaired relaxation to ACh and to NaHS, as well as significantly increased H2S production in lieno-pancreatic artery of LP group. Conclusion: Protein malnutrition resulted in endothelial dysfunction of lieno-pancreatic artery associated with an impaired production and relaxation to H2S, which was restored by TAU. Therefore, beneficial effects of TAU on lieno-pancreatic artery vasodilatory function may result in improved pancreatic islet blood flow highlighting the potential of TAU for vasculo-metabolic protection.Funding: FAPESP, CAPES.


Kanzo ◽  
1977 ◽  
Vol 18 (9) ◽  
pp. 615-624
Author(s):  
Shigeyuki TAKAMORI ◽  
Tatsuro TAKINO ◽  
Takahiro KANATSUNA ◽  
Kazumasu NAKAJIMA ◽  
Yoshio HIRAUMI ◽  
...  

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