Comparison between pre-exercise casein peptide and intact casein supplementation on glucose tolerance in mice fed a high-fat diet

2018 ◽  
Vol 43 (4) ◽  
pp. 355-362 ◽  
Author(s):  
Yutaka Matsunaga ◽  
Yuki Tamura ◽  
Yasuyuki Sakata ◽  
Yudai Nonaka ◽  
Noriko Saito ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Endurance Training ◽  
Soleus Muscle ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Area Under The Curve ◽  
Abdominal Fat ◽  
Oral Glucose ◽  
High Fat

We hypothesized that along with exercise, casein peptide supplementation would have a higher impact on improving glucose tolerance than intact casein. Male 6-week-old ICR mice were provided a high-fat diet to induce obesity and glucose intolerance. The mice were randomly divided into 4 treatment groups: control (Con), endurance training (Tr), endurance training with intact casein supplementation (Cas+Tr), and endurance training with casein peptide supplementation (CP+Tr). The mice in each group were orally administrated water, intact casein, or casein peptide (1.0 mg/g body weight, every day), and then subjected to endurance training (15–25 m/min, 60 min, 5 times/week for 4 weeks) on a motor-driven treadmill 30 min after ingestion. Our results revealed that total intra-abdominal fat was significantly lower in CP+Tr than in Con (p < 0.05). Following an oral glucose tolerance test, the blood glucose area under the curve (AUC) was found to be significantly smaller for CP+Tr than for Con (p < 0.05). Moreover, in the soleus muscle, glucose transporter 4 (GLUT4) protein levels were significantly higher in CP+Tr than in Con (p < 0.01). However, intra-abdominal fat, blood glucose AUC, and GLUT4 protein content in the soleus muscle did not alter in Tr and Cas+Tr when compared with Con. These observations suggest that pre-exercise casein peptide supplementation has a higher effect on improving glucose tolerance than intact casein does in mice fed a high-fat diet.

scholarly journals Effects of Lactobacillus on Mice with Diabetes Induced by High-Fat Diet with Streptozotocin (STZ)

2018 ◽  
Vol 8 (8) ◽  
pp. 1249 ◽  
Author(s):  
Xiaoyong Chen ◽  
Fang Tan ◽  
Ruokun Yi ◽  
Jianfei Mu ◽  
Xin Zhao ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
High Fat Diet ◽  
Glucose Transporter ◽  
Regulatory Element ◽  
Hepatic Insulin Resistance ◽  
Average Weight ◽  
Oral Glucose ◽  
High Fat ◽  
Glut 4 ◽  
Tnf Α

This study aimed to evaluate and compare the effects of heat-killed and live Lactobacillus on mice with diabetes induced by high-fat diet with streptozotocin (STZ). Results based on body weight and liver pathological changes, oral glucose tolerance test, and related serum index (AST (aspartate aminotransferase), ALT (alanine aminotransferase), MDA (malondialdehyde), TNF-α (tumor necrosis factor α), INS (insulin), and GC (glucagon) and gene expression of IL-1β (Interleukin 1β), IRS-1(Insulin receptor substrate 1), GLUT-4 (glucose transporter type 4), PPARγ (peroxisome proliferators-activated receptor γ), and SREBP-1c (sterol-regulatory element-binding protein-1c) levels indicated that Lactobacillus fermentum (LF) and Lactobacillus plantarum (LP) could increase the average weight, alleviate the degree of damage in the liver, and improve the glucose tolerance of mice with diabetes. LF and LP also participated in the downregulation of AST, ALT, MDA, TNF-α, INS, and GC in serum, as well as the inhibition of IL-1β, TNF-α, IRS-1, GLUT-4, PPARγ, and SREBP-1c expression. These regulating effects were remarkable, and the regulating effect of the live group was significantly better than that of the heat-killed group. This study suggested that LF and LP can significantly alleviate liver damage and hepatic insulin resistance in mice with diabetes and that the acting mechanisms of LF and LP were related to cellular components and their activities.

scholarly journals Djulis Hull Improves Insulin Resistance and Modulates the Gut Microbiota in High-Fat Diet (HFD)-Induced Hyperglycaemia

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 45
Author(s):  
Yu-Tang Tung ◽  
Jun-Lan Zeng ◽  
Shang-Tse Ho ◽  
Jin-Wei Xu ◽  
I-Hsuan Lin ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Protein Expression ◽  
Crude Extract ◽  
High Fat Diet ◽  
Insulin Signalling ◽  
Oral Glucose ◽  
Model Assessment ◽  
High Fat

In this study, we annotated the major flavonoid glycoside, rutin, of djulis hull crude extract using a Global Natural Products Social Molecular Networking (GNPS) library and its MS/MS spectra. To evaluate the protective effect of djulis hull crude extract and rutin on glucose tolerance, we fed mice a high-fat diet (HFD) for 16 weeks to induce hyperglycaemia. These results showed that crude extract significantly decreased HFD-induced elevation in the area under the curve (AUC) of weekly random blood glucose and oral glucose tolerance tests (OGTT), homeostasis model assessment (HOMA-IR), and advanced glycation end product (AGE) levels, and significantly increased pIRS1 and Glut4 protein expression in epididymal white adipose tissue (eWAT) and liver. Furthermore, the HFD-induced reduction in the activity of glutathione peroxidase (GPx) and catalase (CAT) was reversed by crude extract. In addition, ZO-1 and occludin protein expression in the colon was markedly downregulated in HFD-fed mice, resulting in decreased intestinal permeability and lipopolysaccharide (LPS) translocation, but were restored following crude extract. Moreover, the crude extract intervention had a profound effect on the alpha diversity and microbial community in the gut microbiota. Therefore, djulis hull crude extract could improve blood glucose and increase insulin receptor sensitivity in HFD-induced hyperglycaemia, which is likely due to its modulation of the gut microbiota, preservation of the integrity of the intestinal barrier to reduce body inflammation, increased antioxidant activity, and modulation of insulin signalling.

scholarly journals Distinct Effects of a High Fat Diet on Bone in Skeletally Mature and Developing Male C57BL/6J Mice

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1666
Author(s):  
Dean S. Ross ◽  
Tzu-Hsuan Yeh ◽  
Shalinie King ◽  
Julia Mathers ◽  
Mark S. Rybchyn ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Bone Formation ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
Age Groups ◽  
Oral Glucose ◽  
Rna Expression ◽  
High Fat ◽  
Mineral Density ◽  
Skeletal Fragility

Increased risks of skeletal fractures are common in patients with impaired glucose handling and type 2 diabetes mellitus (T2DM). The pathogenesis of skeletal fragility in these patients remains ill-defined as patients present with normal to high bone mineral density. With increasing cases of glucose intolerance and T2DM it is imperative that we develop an accurate rodent model for further investigation. We hypothesized that a high fat diet (60%) administered to developing male C57BL/6J mice that had not reached skeletal maturity would over represent bone microarchitectural implications, and that skeletally mature mice would better represent adult-onset glucose intolerance and the pre-diabetes phenotype. Two groups of developing (8 week) and mature (12 week) male C57BL/6J mice were placed onto either a normal chow (NC) or high fat diet (HFD) for 10 weeks. Oral glucose tolerance tests were performed throughout the study period. Long bones were excised and analysed for ex vivo biomechanical testing, micro-computed tomography, 2D histomorphometry and gene/protein expression analyses. The HFD increased fasting blood glucose and significantly reduced glucose tolerance in both age groups by week 7 of the diets. The HFD reduced biomechanical strength, both cortical and trabecular indices in the developing mice, but only affected cortical outcomes in the mature mice. Similar results were reflected in the 2D histomorphometry. Tibial gene expression revealed decreased bone formation in the HFD mice of both age groups, i.e., decreased osteocalcin expression and increased sclerostin RNA expression. In the mature mice only, while the HFD led to a non-significant reduction in runt-related transcription factor 2 (Runx2) RNA expression, this decrease became significant at the protein level in the femora. Our mature HFD mouse model more accurately represents late-onset impaired glucose tolerance/pre-T2DM cases in humans and can be used to uncover potential insights into reduced bone formation as a mechanism of skeletal fragility in these patients.

Abstract 404: NLR Family, Pyrin Domain-containing 3 Knockout Rescues Cardiac Dysfunction Induced by High-fat Diet Feeding

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Matthew R Peterson ◽  
Samantha Haller ◽  
Tracy Ta ◽  
Luiza Bosch ◽  
Aspen Smith ◽  
...  
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Inflammatory Response ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Left Ventricular ◽  
Normal Diet ◽  
High Fat ◽  
Pyrin Domain

NLR family, pyrin domain-containing 3 (NLRP3) is a pattern recognition receptor responsible for perpetuating an inflammatory response through production of pro-inflammatory cytokines IL-1β and IL-18. It has been implicated in the sustained inflammatory response in obesity and multiple cardiovascular disease conditions. In order to investigate NLRP3 as a potential therapeutic target in metabolic syndrome, C57BL/6 wild-type (WT) and NLRP3 knockout (NLRP3-\-) mice were fed a normal diet (ND; 12% fat chow) or a high fat diet (HFD; 45% fat chow) for 5 months. At 5 months, echocardiography and glucose tolerance tests (GTTs) were performed. Cardiac function assessed by fractional shortening (FS) was significantly impaired by HFD feeding in the WT group (0.335 HFD vs. 0.456 ND; p<0.05) but not in the NLRP3-\- (0.449 HFD vs. 0.492 ND; p>0.05). FS was higher in NLRP3-\-HFD than in WT-HFD (p<0.05). Two-dimensional analysis shows the FS difference between NLRP3-\-HFD and WT-HFD was primarily explained by the difference in left ventricular end-systolic dimension (0.2716 cm WT vs. 0.1883 cm NLRP3-\-; p<0.05). Glucose tolerance measured by area under the curve (AUC) was significantly impaired by HFD feeding for both WT (23183 ND vs. 57298 HFD; p<0.001) and NLRP3-\- (23197 ND vs. 44626 HFD; p<0.001), but significantly better in the NLRP3-\-HFD than in WT-HFD (p<0.01). HFD feeding increased fasting blood glucose (FBG) for both WT (97.7 mg . dl -1 ND vs. 164.7 mg . dl -1 HFD; p<0.01) and NLRP3-\- (80.50 mg . dl -1 ND vs. 108.8 mg . dl -1 HFD; p<0.05), but significantly less in NLRP3-\- mice (NLRP3-\- vs. WT; p<0.05). For GTTs, body weight was significantly higher in the WT than NLRP3-\- fed HFD (47.93 g vs. 36.5 g; p<0.001). Body weight explained 92% of variation in glucose tolerance (p<0.0001) and 69% of variation in fasting blood glucose (p<0.0001). WT-HFD averaged 1.31X heavier than NLRP3-\-HFD, while the AUC for the IGTT was 1.28X larger for the WT-HFD than NLRP3-\-HFD. Body weights were not significantly different between genotypes at the time of echo. The results suggest that knockout of NLRP3 may be protective against HFD induced cardiovascular dysfunction. A protective effect on glucose tolerance is not strongly supported.

scholarly journals Glucose Metabolism and Cecal Microbiome Populations Are Improved and Hepatic Biochemical Levels Altered with Consumption of Grape Powder by High-fat Fed C57BL/6 J Mice (P06-024-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Neil Shay ◽  
Marlena Sturm ◽  
Alexandra Becraft ◽  
Rufa Mendez ◽  
Si-Hong Park ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Fasting Blood Glucose ◽  
Area Under The Curve ◽  
Table Grape ◽  
Male Mice ◽  
High Fat ◽  
Grape Skin ◽  
Metabolic Complications ◽  
Powder Consumption

Abstract Objectives Grapes are nutrient-dense, particularly in polyphenolic compounds. Previous research demonstrates benefits of whole grape and grape skin, seed, and polyphenol intake on glucose homeostasis along with other health benefits. We tested the hypothesis that intake of 4 servings per day of table grape would remediate metabolic complications in C57BL/6 J (C57) male mice fed a high-fat diet with added cholesterol and fructose diet modeling an obesogenic and diabetogenic western-style diet. Methods Groups of mice (n = 12) were provided either low-fat plus placebo diet (LF, 10% kcal fat), high-fat plus placebo (HF, 45% kcal fat), or HF plus grape powder (HF + G), for 8 weeks. Grape powder was provided at ∼10% of total energy of diet. C57 mice were provided experimental diets ad libitum. Body weights, food intake, and glucose tolerance were determined. Postmortem, inflammatory markers, cecal microbiome, and the relative concentrations of hepatic metabolites were determined. Results Fasting blood glucose was reduced in the HF + G group compared to HF-fed mice. The glucose tolerance test demonstrated that the Area Under the Curve (AUC) was also reduced. Further, a significant decrease in circulating levels of insulin were observed with HF + G supplementation. The cecal microbiome from HF + G fed mice overlapped with both the HF and LF controls, but also had characteristic shifts that were unique to grape powder consumption. Metabolomic analysis indicated grape consumption impacted inflammation and β-oxidation biomarkers indicating some remediation of hepatic pathologies associated with HF food consumption. The most significantly different hepatic metabolites included grape-derived S-methymethionine and trigonelline, while other murine hepatic metabolites significantly regulated by diet included myo-inositol and 15-HETE. Conclusions Table grape supplementation with a HF western-style diet significantly improved fasting blood glucose, circulating insulin concentrations, and HOMA-IR in C576J/Bl male mice. demonstrating an anti-diabetic effect of grape powder. At modest level of supplementation equivalent to 4 servings/day, grape powder also improved microbiome composition and changed relative levels of specific hepatic metabolites. Up-regulation of 15-HETE by diet suggests grape powder consumption may enhance PPARγ-directed gene expression, consistent with increases in glucose sensitivity observed in this study. Funding Sources California Table Grape Commission.

scholarly journals Patchouli Alcohol from Pogostemon Cablin Prevents Development of Obesity and Improves Glucose Tolerance in High Fat Diet-induced Obese Mice (P06-107-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Jihye Lee ◽  
Seong-Ho Lee
Keyword(s):  
Body Weight ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Oral Glucose ◽  
Male Mice ◽  
Fat Pad ◽  
High Fat ◽  
Patchouli Alcohol ◽  
Brown Adipose ◽  
Pogostemon Cablin

Abstract Objectives Patchouli alcohol is a sesquiterpene alcohol found in Pogostemon cablin. Recently, we observed that patchouli alcohol reduced lipid accumulation in differentiated 3T3-L1 adipocytes and increased glucose uptake in differentiated C2C12 myocytes. This study was designed to investigate anti-obese and anti-diabetic activities of patchouli alcohol using high fat diet-induced obese mouse model. Methods Forty-eight 5-week old C57BL/6 J male mice were assigned into four groups and fed with 1) normal diet (control), 2) high fat diet, 3) high fat diet with gavaging 25 mg of patchouli alcohol/kg body weight and 4) high fat diet with gavaging 50 mg of patchouli alcohol/kg body weight. High fat diet or control diets were provided to each treatment group for four weeks and then different doses of patchouli alcohol (0, 25 or 50 mg/kg body weight) was orally administered for following 8 weeks with the diet. At age of week 17, all animals were sacrificed, fat tissues were collected, and tissue weight was measured. In addition, twenty C57BL/6 J male mice were assigned into the same treatment groups above. At the end of the 8 weeks (age of week 17), the mice were fasted for 12 h and the oral glucose tolerance test was performed after intraperitoneal injection of 2 g of anhydrous glucose/kg body weight. The blood was collected from tail at 0, 15, 30, 90 and 120 min after injection and blood glucose level was analyzed using glucose meter. Results Treatment of patchouli alcohol (50 mg/kg body weight) significantly reduced body weight and accumulation of body fat pads which was highly induced by feeding of high fat diet. An analysis of individual fat pad weights (expressed as mg weight of fat pad/g body weight) revealed a significant decrease of epididymal and retroperitoneal fat pad in patchouli alcohol-treated mice whereas brown adipose tissue were not significantly altered. And, slightly improved glucose tolerance was observed at 90 and 120 minutes after glucose injection in mice treated with patchouli alcohol (50 mg/kg body weight) compared to those fed with high fat diet alone. Conclusions We propose a potential use of patchouli alcohol as an anti-obesity compound in obese population. Funding Sources NIFA Hatch grant. Supporting Tables, Images and/or Graphs

scholarly journals Hypoglycemic effects and mechanisms of electroacupuncture on insulin resistance

2014 ◽  
Vol 307 (3) ◽  
pp. R332-R339 ◽  
Author(s):  
Jieyun Yin ◽  
Jian Kuang ◽  
Manisha Chandalia ◽  
Demidmaa Tuvdendorj ◽  
Batbayar Tumurbaatar ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Free Fatty Acid ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Postprandial Glucose ◽  
Tolerance Test ◽  
High Fat

The aim of this study was to investigate effects and mechanisms of electroacupuncture (EA) on blood glucose and insulin sensitivity in mice fed a high-fat diet. Both wild-type (WT) and adipose ectonucleotide pyrophosphate phosphodiesterase (ENPP1) transgenic (TG) mice were fed a high-fat diet for 12 wk; for each mouse, an intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) were performed with or without EA at abdomen or auricular areas. A high-fat diet-induced insulin resistance in both WT and TG mice. In the WT mice, EA at 3 Hz and 15 Hz, but not at 1 Hz or 100 Hz, via CV4+CV12 significantly reduced postprandial glucose levels; EA at 3 Hz was most potent. The glucose level was reduced by 61.7% at 60 min and 74.5% at 120 min with EA at 3 Hz (all P < 0.001 vs. control). Similar hypoglycemic effect was noted in the TG mice. On the contrary, EA at auricular points increased postprandial glucose level ( P < 0.03). 4). EA at 3 Hz via CV4+CV12 significantly enhanced the decrease of blood glucose after insulin injection, suggesting improvement of insulin sensitivity. Plasma free fatty acid was significantly suppressed by 42.5% at 15 min and 50.8% at 30 min with EA ( P < 0.01) in both WT and TG mice. EA improves glucose tolerance in both WT and TG mice fed a high-fat diet, and the effect is associated with stimulation parameters and acupoints and is probably attributed to the reduction of free fatty acid.

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 Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet

1988 ◽  
Vol 59 (3) ◽  
pp. 373-380 ◽  
Author(s):  
L. M. Morgan ◽  
S. M. Hampton ◽  
J. A. Tredger ◽  
R. Cramb ◽  
V. Marks
Keyword(s):  
Glucose Tolerance ◽  
Energy Intake ◽  
Plasma Glucose ◽  
High Fat Diet ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Fat Intake ◽  
High Fat ◽  
C Peptide ◽  
Glucose Levels

1. Five healthy volunteers (usual fat intake 103) (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose.2. Subjects increased their fat intake by 68 (SE 9·6) % for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)).3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured.4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0–180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P < 0·05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P < 0·01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0–180 min, following oral glucose 6·7 (SE 0·3) mmol/l.h for control and 4·2 (SE 0·6) mmol/l.h for HFD; P < 0·01).5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance.6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine.

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