Egg white hydrolysate enhances insulin sensitivity in high-fat diet-induced insulin-resistant rats via Akt activation

2019 ◽  
Vol 122 (1) ◽  
pp. 14-24 ◽  
Author(s):  
F. Jahandideh ◽  
S. C. de Campos Zani ◽  
M. Son ◽  
S. D. Proctor ◽  
S. T. Davidge ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Egg White ◽  
Oral Glucose ◽  
Protein Abundance ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Insulin Resistant

AbstractAgents that block the renin–angiotensin system (RAS) improve glucoregulation in the metabolic syndrome disorder. We evaluated the effects of egg white hydrolysate (EWH), previously shown to modulate the protein abundance of RAS component in vivo, on glucose homeostasis in diet-induced insulin-resistant rats. Sprague–Dawley rats were fed a high-fat diet (HFD) for 6 weeks to induce insulin resistance. They were then randomly divided into four groups receiving HFD or HFD supplemented with different concentrations of EWH (1, 2 and 4 %) for another 6 weeks in the first trial. In the second trial, insulin-resistant rats were divided into two groups receiving only HFD or HFD+4 % EWH for 6 weeks. Glucose homeostasis was assessed by oral glucose tolerance and insulin tolerance tests. Insulin signalling and protein abundance of RAS components, gluconeogenesis enzymes and PPARγ were evaluated in muscle, fat and liver. Adipocyte morphology and inflammatory markers were evaluated. In vivo administration of EWH increased insulin sensitivity, improved oral glucose tolerance (P < 0·0001) and reduced systemic inflammation (P < 0·05). EWH potentiated insulin-induced Akt phosphorylation in muscle (P = 0·0341) and adipose tissue (P = 0·0276), but minimal differences in the protein abundance of tissue RAS components between the EWH and control groups were observed. EWH treatment also reduced adipocyte size (P = 0·0383) and increased PPARγ2 protein abundance (P = 0·0237). EWH treatment yielded positive effects on the inflammatory profile, glucose tolerance, insulin sensitivity and adipocyte differentiation in HFD-induced insulin resistance rats. The involvement of local RAS activity requires further investigation.

scholarly journals Germline or inducible knockout of p300 or CBP in skeletal muscle does not alter insulin sensitivity

2019 ◽  
Vol 316 (6) ◽  
pp. E1024-E1035 ◽  
Author(s):  
Vitor F. Martins ◽  
Jessica R. Dent ◽  
Kristoffer Svensson ◽  
Shahriar Tahvilian ◽  
Maedha Begur ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Binding Protein ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Skeletal Muscle Insulin Sensitivity

Akt is a critical mediator of insulin-stimulated glucose uptake in skeletal muscle. The acetyltransferases, E1A binding protein p300 (p300) and cAMP response element-binding protein binding protein (CBP) are phosphorylated and activated by Akt, and p300/CBP can acetylate and inactivate Akt, thus giving rise to a possible Akt-p300/CBP axis. Our objective was to determine the importance of p300 and CBP to skeletal muscle insulin sensitivity. We used Cre-LoxP methodology to generate mice with germline [muscle creatine kinase promoter (P-MCK and C-MCK)] or inducible [tamoxifen-activated, human skeletal actin promoter (P-iHSA and C-iHSA)] knockout of p300 or CBP. A subset of P-MCK and C-MCK mice were switched to a calorie-restriction diet (60% of ad libitum intake) or high-fat diet at 10 wk of age. For P-iHSA and C-iHSA mice, knockout was induced at 10 wk of age. At 13–15 wk of age, we measured whole-body energy expenditure, oral glucose tolerance, and/or ex vivo skeletal muscle insulin sensitivity. Although p300 and CBP protein abundance and mRNA expression were reduced 55%–90% in p300 and CBP knockout mice, there were no genotype differences in energy expenditure or fasting glucose and insulin concentrations. Moreover, neither loss of p300 or CBP impacted oral glucose tolerance or skeletal muscle insulin sensitivity, nor did their loss impact alterations in these parameters in response to a calorie restriction or high-fat diet. Muscle-specific loss of either p300 or CBP, be it germline or in adulthood, does not impact energy expenditure, glucose tolerance, or skeletal muscle insulin action.

Effects of a Seven Day High-Fat Diet on Oral Glucose Tolerance and Endothelial Function in Young Males

2015 ◽  
Vol 47 ◽  
pp. 289-290
Author(s):  
Cody G. Durrer ◽  
Zhongxiao Wan ◽  
Nia Lewis ◽  
Philip N. Ainslie ◽  
Nathan T. Jenkins ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Endothelial Function ◽  
High Fat Diet ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Young Males

scholarly journals β-cell knockout of SENP1 reduces responses to incretins and worsens oral glucose tolerance in high fat diet-fed mice

2021 ◽  
Author(s):  
Haopeng Lin ◽  
Nancy Smith ◽  
Aliya F Spigelman ◽  
Kunimasa Suzuki ◽  
Mourad Ferdaoussi ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Glucagon Secretion ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Β Cell ◽  
Islet Mass

SUMOylation reduces oxidative stress and preserves islet mass at the expense of robust insulin secretion. To investigate a role for the deSUMOylating enzyme <u>sen</u>trin-specific <u>p</u>rotease <u>1</u> (SENP1) following metabolic stress, we put pancreas/gut-specific SENP1 knockout mice (pSENP1-KO) on a high fat diet (HFD). Male pSENP1-KO mice were more glucose intolerant following HFD than littermate controls, but only in response to oral glucose. A similar phenotype was observed in females. Plasma glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like-peptide 1 (GLP-1) responses were identical in pSENP1-KO and -WT littermates, including the HFD-induced upregulation of GIP responses. Islet mass was not different, but insulin secretion and β-cell exocytotic responses to the GLP-1 receptor agonist Exendin-4 (Ex4) and GIP were impaired in islets lacking SENP1. Glucagon secretion from pSENP1-KO islets was also reduced, so we generated β-cell-specific SENP1 knockout mice (βSENP1-KO). These phenocopied the pSENP1-KO mice with selective impairment in oral glucose tolerance following HFD, preserved islet mass expansion, and impaired β-cell exocytosis and insulin secretion to Ex4 and GIP without changes in cAMP or Ca<sup>2+</sup> levels. Thus, β-cell SENP1 limits oral glucose intolerance following HFD by ensuring robust insulin secretion at a point downstream of incretin signaling.

scholarly journals β-Cell Knockout of SENP1 Reduces Responses to Incretins and Worsens Oral Glucose Tolerance in High Fat Diet-Fed Mice

Diabetes ◽  
2021 ◽  
pp. db201235
Author(s):  
Haopeng Lin ◽  
Nancy Smith ◽  
Aliya F Spigelman ◽  
Kunimasa Suzuki ◽  
Mourad Ferdaoussi ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
High Fat Diet ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Β Cell

scholarly journals β-Cell Glucagon-Like Peptide-1 Receptor Contributes to Improved Glucose Tolerance After Vertical Sleeve Gastrectomy

Endocrinology ◽  
2016 ◽  
Vol 157 (9) ◽  
pp. 3405-3409 ◽  
Author(s):  
Darline Garibay ◽  
Anne K. McGavigan ◽  
Seon A. Lee ◽  
James V. Ficorilli ◽  
Amy L. Cox ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
High Fat Diet ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Vertical Sleeve Gastrectomy ◽  
High Fat ◽  
Β Cell ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Glucose Stimulated Insulin Secretion

Vertical sleeve gastrectomy (VSG) produces high rates of type 2 diabetes remission; however, the mechanisms responsible for this remain incompletely defined. Glucagon-like peptide-1 (GLP-1) is a gut hormone that contributes to the maintenance of glucose homeostasis and is elevated after VSG. VSG-induced increases in postprandial GLP-1 secretion have been proposed to contribute to the glucoregulatory benefits of VSG; however, previous work has been equivocal. In order to test the contribution of enhanced β-cell GLP-1 receptor (GLP-1R) signaling we used a β-cell-specific tamoxifen-inducible GLP-1R knockout mouse model. Male β-cell-specific Glp-1rβ-cell+/+ wild type (WT) and Glp-1rβ-cell−/− knockout (KO) littermates were placed on a high-fat diet for 6 weeks and then switched to high-fat diet supplemented with tamoxifen for the rest of the study. Mice underwent sham or VSG surgery after 2 weeks of tamoxifen diet and were fed ad libitum postoperatively. Mice underwent oral glucose tolerance testing at 3 weeks and were euthanized at 6 weeks after surgery. VSG reduced body weight and food intake independent of genotype. However, glucose tolerance was only improved in VSG WT compared with sham WT, whereas VSG KO had impaired glucose tolerance relative to VSG WT. Augmentation of glucose-stimulated insulin secretion during the oral glucose tolerance test was blunted in VSG KO compared with VSG WT. Therefore, our data suggest that enhanced β-cell GLP-1R signaling contributes to improved glucose regulation after VSG by promoting increased glucose-stimulated insulin secretion.

scholarly journals β-cell knockout of SENP1 reduces responses to incretins and worsens oral glucose tolerance in high fat diet-fed mice

2021 ◽  
Author(s):  
Haopeng Lin ◽  
Nancy Smith ◽  
Aliya F Spigelman ◽  
Kunimasa Suzuki ◽  
Mourad Ferdaoussi ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Glucagon Secretion ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
High Fat ◽  
Β Cell ◽  
Islet Mass

SUMOylation reduces oxidative stress and preserves islet mass at the expense of robust insulin secretion. To investigate a role for the deSUMOylating enzyme <u>sen</u>trin-specific <u>p</u>rotease <u>1</u> (SENP1) following metabolic stress, we put pancreas/gut-specific SENP1 knockout mice (pSENP1-KO) on a high fat diet (HFD). Male pSENP1-KO mice were more glucose intolerant following HFD than littermate controls, but only in response to oral glucose. A similar phenotype was observed in females. Plasma glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like-peptide 1 (GLP-1) responses were identical in pSENP1-KO and -WT littermates, including the HFD-induced upregulation of GIP responses. Islet mass was not different, but insulin secretion and β-cell exocytotic responses to the GLP-1 receptor agonist Exendin-4 (Ex4) and GIP were impaired in islets lacking SENP1. Glucagon secretion from pSENP1-KO islets was also reduced, so we generated β-cell-specific SENP1 knockout mice (βSENP1-KO). These phenocopied the pSENP1-KO mice with selective impairment in oral glucose tolerance following HFD, preserved islet mass expansion, and impaired β-cell exocytosis and insulin secretion to Ex4 and GIP without changes in cAMP or Ca<sup>2+</sup> levels. Thus, β-cell SENP1 limits oral glucose intolerance following HFD by ensuring robust insulin secretion at a point downstream of incretin signaling.

Short-Term High-Fat Diet Alters Substrate Utilization during Exercise but Not Glucose Tolerance in Highly Trained Athletes

2001 ◽  
Vol 11 (3) ◽  
pp. 273-286 ◽  
Author(s):  
Heidi M. Staudacher ◽  
Andrew L. Carey ◽  
Nicola K. Cummings ◽  
John A. Hawley ◽  
Louise M. Burke
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Dietary Intervention ◽  
Substrate Oxidation ◽  
Whole Body ◽  
Oral Glucose ◽  
High Fat ◽  
Short Term ◽  
Time Curve

We determined the effect of a high-fat diet and carbohydrate (CHO) restoration on substrate oxidation and glucose tolerance in 7 competitive ultra-endurance athletes (peak oxygen uptake [V̇O2peak] 68 ± 1 ml · kg−1 · min−1; mean±SEM). For 6 days, subjects consumed a random order of a high-fat (69% fat; FAT-adapt) or a high-CHO (70% CHO; HCHO) diet, each followed by 1 day of a high-CHO diet. Treatments were separated by an 18-day wash out. Substrate oxidation was determined during submaximal cycling (20 min at 65% V̇O2peak) prior to and following the 6 day dietary interventions. Fat oxidation at baseline was not different between treatments (17.4 ± 2.1 vs. 16.1 ± 1.3 g · 20 min−1 for FAT-adapt and HCHO, respectively) but increased 34% after 6 days of FAT-adapt (to 23.3 ± 0.9 g · 20 min−1, p < .05) and decreased 30% after HCHO (to 11.3±1.4 g · 20 min−1, p < .05). Glucose tolerance, determined by the area under the plasma [glucose] versus time curve during an oral glucose tolerance (OGTT) test, was similar at baseline (545±21 vs. 520±28 mmol · L−1 · 90 min−1), after 5-d of dietary intervention (563 ± 26 vs. 520 ± 18 mmol · L−1 · 90 min−1) and after 1 d of high-CHO (491 ± 28 vs. 489 ± 22 mmol · L−1 · 90min−1 for FAT- adapt and HCHO, respectively). An index of whole-body insulin sensitivity (SI 10000/÷fasting [glucose] × fasting [insulin] × mean [glucose] during OGTT × mean [insulin] during OGTT) was similar at baseline (15 ± 2 vs. 17 ± 5 arbitrary units), after 5-d of dietary intervention (15 ± 2 vs. 15 ± 2) and after 24 h of CHO loading (17 ± 3 vs. 18 ± 2 for FAT- adapt and HCHO, respectively). We conclude that despite marked changes in the pattern of substrate oxidation during submaximal exercise, short-term adaptation to a high-fat diet does not alter whole-body glucose tolerance or an index of insulin sensitivity in highly-trained individuals.

Sign in / Sign up

Export Citation Format

Share Document