Dietary supplementation with vitamin E and C attenuates dexamethasone-induced glucose intolerance in rats

2012 ◽  
Vol 302 (1) ◽  
pp. R49-R58 ◽  
Author(s):  
Deon B. Williams ◽  
Zhongxiao Wan ◽  
Bruce C. Frier ◽  
Rhonda C. Bell ◽  
Catherine J. Field ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin E ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Alpha Tocopherol ◽  
Dietary Vitamin ◽  
Acid Oxidation ◽  
Mitochondrial Enzymes ◽  
Ampk Signaling ◽  
Vitamin E And C

Glucocorticoid excess induces marked insulin resistance and glucose intolerance. A recent study has shown that antioxidants prevent dexamethasone (DEX)-induced insulin resistance in cultured adipocytes. The purpose of this investigation was to examine the effects of dietary vitamin E and C (Vit E/C) supplementation on DEX-induced glucose intolerance in rats. We hypothesized that feeding rats a diet supplemented with Vit E/C would improve glucose tolerance and restore insulin signaling in skeletal muscle, adipose, and liver and prevent alterations in AMPK signaling in these tissues. Male Wistar rats received either a control or Vit E/C-supplemented diet (0.5 g/kg diet each of l-ascorbate and dl-all rac-alpha-tocopherol) for 9 days prior to, and during, 5 days of daily DEX treatment (subcutaneous injections 0.8 mg/g body wt). DEX treatment resulted in increases in the glucose and insulin area under the curve (AUC) during an intraperitoneal glucose tolerance test. The glucose, but not insulin, AUC was lowered with Vit E/C supplementation. Improvements in glucose tolerance occurred independent of a restoration of PKB phosphorylation in tissues of rats stimulated with an intraperitoneal injection of insulin but were associated with increases in AMPK signaling in muscle and reductions in AMPK signaling and the expression of fatty acid oxidation enzymes in liver. There were no differences in mitochondrial enzymes in triceps muscles between groups. This study is the first to report that dietary Vit E/C supplementation can partially prevent DEX-induced glucose intolerance in rats.

scholarly journals Effects of Vitamin E and Vitamin C on Mercury Induced Toxicity in Mice

2013 ◽  
Vol 19 (2) ◽  
pp. 93-100 ◽  
Author(s):  
MA Huq ◽  
MA Awal ◽  
M Mostofa ◽  
A Ghosh ◽  
AR Das
Keyword(s):  
Body Weight ◽  
Vitamin E ◽  
Vitamin C ◽  
Biochemical Parameters ◽  
Hematological Parameters ◽  
Protective Role ◽  
Alpha Tocopherol ◽  
Post Mortem ◽  
Group B ◽  
Vitamin E And C

The present study was undertaken to find out the efficacy of vitamin E and/or vitamin C against mercury (Hg) induced toxicity in mice. Sixty mice were randomly divided into 5 equal groups (n=12). One group of mice (Group A) was kept as control and each of rest four groups (B, C, D and E) were fed with mercuric chloride (HgCl2) in drinking water @ 65 mg/L. In addition to HgCl2 alpha-tocopherol (vitamin E) @ 100 mg/L, ascorbic acid (vitamin C) @ 250 mg/L and combination of vitamin E and vitamin C at same dose were given to the mice of groups C, D and E respectively. All treatments were continued for 28 consecutive days. Four mice of each group were sacrificed on day 1, 14 and 28 and efficacy of vitamin E and vitamin C against Hg induced toxicity were evaluated by observing toxic signs, body weight, hemato-biochemical parameters and postmortem lesions. Mild (++) toxic signs as evident by reduced feed and water intake, salivation, vomiting, excitement, muscle tremor, ataxia, restlessness, incordination and ruffled hair coat were observed from 2nd week (group B) and from 3rd week (group C and D) by intoxication with HgCl2. Significant (P<0.01) reduction of body weight (18.38%) and hematological parameters i.e. TEC (19.88%), TLC (27.89%), Hb content (34.09%) and PCV (9.15%) were observed at day 28 in HgCl2 induced intoxicated mice (group B). At identical period in same group biochemical parameters i.e. AST (46.99%) and ALT (58.72%) increased significantly (p<0.01). Pinpoint hemorrhages throughout the liver and highly (++++) congested kidney was also observed at post mortem (group B). All the parameters i.e. toxic signs, body weight, hemato-biochemical and post mortem lesions were found to be slight (+) or mild (++) and/or improved in rest three groups of mice following treatment with vitamin E, vitamin C and combination of vitamin E and vitamin C. The present study reveals that vitamin E and C have a protective role against Hg poisoning. However, combination of vitamin E and C gave better results.DOI: http://dx.doi.org/10.3329/pa.v19i2.16949 Progress. Agric. 19(2): 93 - 100, 2008

Insulin resistance caused by amylin in conscious rats is independent of induced hypocalcemia and fades during long-term exposure

1993 ◽  
Vol 129 (4) ◽  
pp. 360-365 ◽  
Author(s):  
Clemens Fürnsinn ◽  
Peter Nowotny ◽  
Michael Roden ◽  
Madeleine Rohac ◽  
Thomas Pieber ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Tolerance Test ◽  
Zucker Rats ◽  
Control Group ◽  
Short Term ◽  
Euglycemic Hyperinsulinemic Clamp

To compare the effect of short- vs long-term amylin infusion on insulin sensitivity, glucose tolerance and serum calcemia, euglycemic-hyperinsulinemic clamp (26 pmol·kg−1·min−1) and glucose tolerance tests (2.4 mmol/kg over 30 min) were performed in lean Zucker rats. Three infusion protocols were employed: control group: 24 h of iv saline; short-term amylin exposure: 22 h of iv saline followed by 2 h of iv amylin (20 μg/h); long-term amylin exposure: 24 h of iv amylin (20 μg/h). Insulin resistance was induced by short-term amylin infusion during euglycemic clamping, as shown by a 41% decrease in space-corrected glucose infusion rates (μmol·kg−1·min−1; control group, 106.0±15.0; short-term iv amylin, 62.7±15.0; p<0.00 5). After long-term amylin exposure, insulin sensitivity was identical to control values (109.9±6.7). This fading action of amylin was confirmed by data from the glucose tolerance test, demonstrating glucose intolerance after short- but not after long-term amylin exposure. Serum calcium concentration decreased during short-term (2 h) amylin infusion (from 2.52±0.15 to 2.09±0.12 mmol/l; p<0.01) and hypocalcemia of a similar extent also was present after 22 h and 24 h of amylin exposure (2.10±0.09 and 2.04±0.14 mmol/l, respectively). The data demonstrate that short-term amylin infusion induces insulin resistance and glucose intolerance, both of which vanish during long-term (>22 h) amylin exposure, being apparently independent of induced hypocalcemia.

scholarly journals Selenium and α-tocopherol content in eggs produced by hens that were fed diets supplemented with selenomethionine, sodium selenite and vitamin E

2010 ◽  
Vol 55 (No. 9) ◽  
pp. 388-397 ◽  
Author(s):  
M. Skřivan ◽  
I. Bubancová ◽  
M. Marounek ◽  
G. Dlouhá
Keyword(s):  
Vitamin E ◽  
Sodium Selenite ◽  
Thiobarbituric Acid ◽  
Basal Diet ◽  
Tocopherol Content ◽  
Alpha Tocopherol ◽  
Dietary Vitamin ◽  
Tocopherol Concentration ◽  
The Third ◽  
Egg Yolks

The effect of supplementing dietary selenium (Se) and vitamin E was investigated in 330 24-week-old laying hens. The hens were fed a basal diet containing Se and &alpha;-tocopherol at 0.11 and 26 mg/kg, respectively, or a diet supplemented with Se at 0.3 mg/kg and vitamin E between 0 and 625 mg/kg. Se was supplied as Se-methionine or sodium selenite. The eggs were collected for analysis during the third, seventh and eleventh weeks of the experiment. Supplementation of either form of Se significantly increased the Se concentration in egg yolks and whites, with a more pronounced effect caused by Se-methionine. The egg yolk &alpha;-tocopherol concentration paralleled the dietary &alpha;-tocopherol concentration. At a high dietary &alpha;-tocopherol concentration (632 mg/kg), the retinol content in egg yolks from hens fed Se-methionine increased significantly. Supplementation of Se-methionine significantly increased the &alpha;-tocopherol content in the eggs in the third and seventh weeks of the experiment. A moderate decrease in yolk cholesterol was observed in hens fed Se-methionine and &alpha;-tocopherol at 119 mg/kg. The concentration of products from lipid peroxidation (thiobarbituric acid-reactive substances, TBARS) in egg yolks increased marginally during the refrigerated storage of the eggs for 2 weeks. The effect of dietary vitamin E on TBARS formation was generally small, although a more significant effect was observed at the highest dose tested.

scholarly journals Altered body composition and energy expenditure but normal glucose tolerance among humans with a long-chain fatty acid oxidation disorder

2013 ◽  
Vol 305 (10) ◽  
pp. E1299-E1308 ◽  
Author(s):  
Melanie B. Gillingham ◽  
Cary O. Harding ◽  
Dale A. Schoeller ◽  
Dietrich Matern ◽  
Jonathan Q. Purnell
Keyword(s):  
Insulin Resistance ◽  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Total Energy Expenditure ◽  
Acid Oxidation ◽  
Hmw Adiponectin ◽  
Normal Glucose ◽  
Lchad Deficiency ◽  
Long Chain

The development of insulin resistance has been associated with impaired mitochondrial fatty acid oxidation (FAO), but the exact relationship between FAO capacity and glucose metabolism continues to be debated. To address this controversy, patients with long-chain 3-hydroxy acyl-CoA dehydrogenase (LCHAD) deficiency underwent an oral glucose tolerance test (OGTT) and measurement of energy expenditure, body composition, and plasma metabolites. Compared with controls, patients with LCHAD deficiency had a trend toward higher total body fat and extramyocellular lipid deposition but similar levels of intramyocelluar and intrahepatic lipids. Resting energy expenditure was similar between the groups, but respiratory quotient was higher and total energy expenditure was lower in LCHAD-deficient patients compared with controls. High-molecular-weight (HMW) adiponectin levels were lower and plasma long-chain acylcarnitines were higher among LCHAD-deficient patients. Fasting and post-OGTT levels of glucose, insulin, and ghrelin, along with estimates of insulin sensitivity, were the same between the groups. Despite decreased capacity for FAO, lower total energy expenditure and plasma HMW adiponectin, and increased plasma acylcarnitines, LCHAD-deficient patients exhibited normal glucose tolerance. These data suggest that inhibition of the FAO pathway in humans is not sufficient to induce insulin resistance.

Naringin improves zidovudine- and stavudine-induced skeletal muscle complications in rats

2016 ◽  
Vol 36 (1) ◽  
pp. 93-105 ◽  
Author(s):  
OO Adebiyi ◽  
OA Adebiyi ◽  
PMO Owira
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Vitamin E ◽  
Protein Expression ◽  
Hiv Infection ◽  
Glucose Intolerance ◽  
B Cell Lymphoma ◽  
Oral Glucose ◽  
Management Options ◽  
Carbonyl Protein

Chronic use of nucleoside reverse transcriptase inhibitors (NRTIs) in managing human immunodeficiency virus (HIV) infection has been associated with several complications. Available management options for these complications have yielded controversial results, thus the need to urgently find newer alternatives. Naringin, a plant-derived flavonoid, has been shown to possess antioxidant and antiapoptotic properties which can be exploited in managing NRTI-induced complications. This study therefore investigated the effects of naringin on some NRTI-induced complications. Forty-nine rats (200–250 g) were divided into seven groups and were orally treated with stavudine (d4T)-only, d4T + naringin, d4T + vitamin E, zidovudine (AZT)-only, AZT + naringin, AZT + vitamin E, and distilled water, respectively. Drugs were administered once daily for 56 days, and oral glucose tolerance tests conducted on day 54 of the experiments and rats were thereafter sacrificed on day 56 by halothane overdose. Plasma samples and the left gastrocnemius muscles were stored at −80°C for further analysis. There was significant glucose intolerance, insulin resistance, oxidative stress, and apoptosis in the skeletal muscles of AZT- or d4T-only–treated rats. Naringin, however, significantly reduced fasting blood glucose and fasting plasma insulin concentrations, mitigated glucose intolerance, and insulin resistance in addition to reducing malondialdehyde and carbonyl protein concentrations when coadministered with either NRTIs. Furthermore, naringin improved antioxidant enzyme activities, reduced skeletal muscle BCL-2-associated X protein expression, and improved B-cell lymphoma-2 protein expression compared to AZT- or d4T-only–treated rats. Naringin ameliorated AZT- and d4T-induced complications and therefore should be further investigated as a possible nutritional supplement in managing HIV infection.

scholarly journals Saturated- and n-6 Polyunsaturated-Fat Diets Each Induce Ceramide Accumulation in Mouse Skeletal Muscle: Reversal and Improvement of Glucose Tolerance by Lipid Metabolism Inhibitors

Endocrinology ◽  
2010 ◽  
Vol 151 (9) ◽  
pp. 4187-4196 ◽  
Author(s):  
G. Frangioudakis ◽  
J. Garrard ◽  
K. Raddatz ◽  
J. L. Nadler ◽  
T. W. Mitchell ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
De Novo ◽  
Saturated Fat ◽  
Tolerance Test ◽  
Polyunsaturated Fat ◽  
Unsaturated Fat ◽  
Fat Diets

Lipid-induced insulin resistance is associated with intracellular accumulation of inhibitory intermediates depending on the prevalent fatty acid (FA) species. In cultured myotubes, ceramide and phosphatidic acid (PA) mediate the effects of the saturated FA palmitate and the unsaturated FA linoleate, respectively. We hypothesized that myriocin (MYR), an inhibitor of de novo ceramide synthesis, would protect against glucose intolerance in saturated fat-fed mice, while lisofylline (LSF), a functional inhibitor of PA synthesis, would protect unsaturated fat-fed mice. Mice were fed diets enriched in saturated fat, n-6 polyunsaturated fat, or chow for 6 wk. Saline, LSF (25 mg/kg · d), or MYR (0.3 mg/kg · d) were administered by mini-pumps in the final 4 wk. Glucose homeostasis was examined by glucose tolerance test. Muscle ceramide and PA were analyzed by mass spectrometry. Expression of LASS isoforms (ceramide synthases) was evaluated by immunoblotting. Both saturated and polyunsaturated fat diets increased muscle ceramide and induced glucose intolerance. MYR and LSF reduced ceramide levels in saturated and unsaturated fat-fed mice. Both inhibitors also improved glucose tolerance in unsaturated fat-fed mice, but only LSF was effective in saturated fat-fed mice. The discrepancy between ceramide and glucose tolerance suggests these improvements may not be related directly to changes in muscle ceramide and may involve other insulin-responsive tissues. Changes in the expression of LASS1 were, however, inversely correlated with alterations in glucose tolerance. The demonstration that LSF can ameliorate glucose intolerance in vivo independent of the dietary FA type indicates it may be a novel intervention for the treatment of insulin resistance.

scholarly journals Glucose Intolerance, Insulin Resistance, and Hyperandrogenemia in First Degree Relatives of Women with Polycystic Ovary Syndrome

2003 ◽  
Vol 88 (5) ◽  
pp. 2031-2036 ◽  
Author(s):  
Bülent O. Yildiz ◽  
Hakan Yarali ◽  
Havva Oguz ◽  
Miyase Bayraktar
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Matched Control ◽  
Polycystic Ovary ◽  
Family Members ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Ovary Syndrome ◽  
First Degree Relatives

Polycystic ovary syndrome (PCOS) is associated with hyperinsulinemia, insulin resistance (IR), increased risk of glucose intolerance, and type 2 diabetes. Family studies have indicated a genetic susceptibility to PCOS. The aims of this study were 1) to assess glucose tolerance status, gonadotropins, and androgens in first degree relatives of patients with PCOS; and 2) to assess IR in normal glucose tolerant (NGT) family members. One hundred two family members of 52 patients with PCOS [MothersPCOS (n = 34; mean age, 46.5 yr; mean body mass index (BMI), 28.8 kg/m2), FathersPCOS (n = 24; mean age, 50.4 yr; mean BMI, 27.5 kg/m2), SistersPCOS (n = 19; mean age, 25.1 yr; mean BMI, 22.9 kg/m2), and BrothersPCOS (n = 25; mean age, 23.7 yr; mean BMI, 22.5 kg/m2)] and 82 unrelated healthy control subjects without a family history of diabetes or PCOS (4 age- and weight-matched subgroups, i.e. ControlMothersPCOS, ControlFathersPCOS, ControlSistersPCOS, and ControlBrothersPCOS) were studied. Glucose and insulin (at baseline and during a 75-g, 2-h oral glucose tolerance test) were measured. IR was assessed by fasting insulin (FI), fasting glucose to insulin ratio (FGI), homeostatic model assessment (HOMA IR), and area under the curve for insulin during the oral glucose tolerance test (AUCinsulin) in NGT MothersPCOS, FathersPCOS, SistersPCOS, BrothersPCOS, and matched control subgroups. Including the prestudy-diagnosed 3 mothers and 2 fathers with diabetes, diabetes and impaired glucose tolerance (IGT) were noted in 16% and 30% of MothersPCOS and 27% and 31% of FathersPCOS, respectively. There was no diabetes in SistersPCOS and BrothersPCOS. IGT was found in 5% of SistersPCOS. Impaired fasting glucose was found in 3% of MothersPCOS and 4% of BrothersPCOS. The analysis of NGT family members showed that MothersPCOS had higher FI (P &lt; 0.05), HOMA IR (P &lt; 0.05), and AUCinsulin (P &lt; 0.01) and lower FGI (P &lt; 0.05) than ControlMothersPCOS, whereas all IR parameters were comparable between FathersPCOS and their matched control subgroup. SistersPCOS had higher FI (P &lt; 0.05), HOMA IR (P &lt; 0.01), and AUCinsulin (P &lt; 0.05) and lower FGI (P &lt; 0.01), and BrothersPCOS had higher AUCinsulin (P &lt; 0.01) than their matched control subgroups, respectively. MothersPCOS had higher testosterone levels than ControlMothersPCOS (P &lt; 0.01 and P &lt; 0.05 for pre- and postmenopausal women, respectively). SistersPCOS had higher LH (P &lt; 0.01), testosterone (P &lt; 0.001), androstenedione (P &lt; 0.01), and dehydroepiandrosterone sulfate (P &lt; 0.05) levels than ControlSistersPCOS. There was no difference in gonadotropin and androgen levels in FathersPCOS compared with ControlFathersPCOS or in BrothersPCOS compared with ControlBrothersPCOS. Our results suggest that 1) first degree relatives of patients with PCOS may be at high risk for diabetes and glucose intolerance; 2) NGT female family members have insulin resistance; and 3) mothers and sisters of PCOS patients have higher androgen levels than control subjects. We propose that the high risks of these impairments warrant screening in first degree relatives of patients with PCOS.

scholarly journals Long-term dysbiosis promotes insulin resistance during obesity despite rapid diet-induced changes in the gut microbiome of mice

2017 ◽  
Author(s):  
Kevin P. Foley ◽  
Emmanuel Denou ◽  
Brittany M. Duggan ◽  
Rebecca Chan ◽  
Jennifer C. Stearns ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Intestinal Microbiota ◽  
Fecal Microbiota ◽  
Taxonomic Composition ◽  
Short Term ◽  
Fecal Microbiome ◽  
Induced Changes

AbstractThe intestinal microbiota and insulin sensitivity are rapidly altered in response to a high fat diet (HFD). It is unclear if gut dysbiosis precedes insulin resistance or vice versa. The initial triggers of diet-induced insulin resistance can differ from mechanisms underlying chronic dysglycemia during prolonged obesity. It is not clear if intestinal dysbiosis contributes to insulin resistance during short-term or long-term HFD-feeding. We found that diet-induced changes in the composition of the fecal microbiome preceded changes in glucose and insulin tolerance at both the onset and removal of a HFD in mice. Dysbiosis occurred after 1-3 days of HFD-feeding, whereas insulin and glucose intolerance manifested by 3-4 days. Antibiotic treatment did not alter glucose tolerance during this short-term HFD period. Conversely, antibiotics improved glucose tolerance in mice with protracted obesity caused by long-term HFD feeding for over 2 months. We also found that microbiota transmissible glucose intolerance only occurred after prolonged diet-induced dysbiosis. Germ-free mice had impaired glucose tolerance when reconstituted with the microbiota from long-term, but not short-term HFD-fed animals. Our results are consistent with intestinal microbiota contributing to chronic insulin resistance and dysglycemia during prolonged obesity, despite rapid diet-induced changes in the taxonomic composition of the fecal microbiota.

scholarly journals Comparing the Fasting and Random-Fed Metabolome Response to an Oral Glucose Tolerance Test in Children and Adolescents: Implications of Sex, Obesity, and Insulin Resistance

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3365
Author(s):  
Jennifer L. LaBarre ◽  
Emily Hirschfeld ◽  
Tanu Soni ◽  
Maureen Kachman ◽  
Janis Wigginton ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Acid Oxidation ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Nutrient Metabolism

As the incidence of obesity and type 2 diabetes (T2D) is occurring at a younger age, studying adolescent nutrient metabolism can provide insights on the development of T2D. Metabolic challenges, including an oral glucose tolerance test (OGTT) can assess the effects of perturbations in nutrient metabolism. Here, we present alterations in the global metabolome in response to an OGTT, classifying the influence of obesity and insulin resistance (IR) in adolescents that arrived at the clinic fasted and in a random-fed state. Participants were recruited as lean (n = 55, aged 8–17 years, BMI percentile 5–85%) and overweight and obese (OVOB, n = 228, aged 8–17 years, BMI percentile ≥ 85%). Untargeted metabolomics profiled 246 annotated metabolites in plasma at t0 and t60 min during the OGTT. Our results suggest that obesity and IR influence the switch from fatty acid (FA) to glucose oxidation in response to the OGTT. Obesity was associated with a blunted decline of acylcarnitines and fatty acid oxidation intermediates. In females, metabolites from the Fasted and Random-Fed OGTT were associated with HOMA-IR, including diacylglycerols, leucine/isoleucine, acylcarnitines, and phosphocholines. Our results indicate that at an early age, obesity and IR may influence the metabolome dynamics in response to a glucose challenge.

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