scholarly journals Late introduction of low dose resveratrol and grape powder after estradiol depletion does not restore glucose tolerance in the ovariectomized rat.

2018 ◽  
Vol 8 (2) ◽  
pp. 79
Author(s):  
Eoin Anderson ◽  
Dan Cervone ◽  
David James Dyck
Keyword(s):  
Glucose Tolerance ◽  
Body Mass ◽  
Glucose Intolerance ◽  
Low Dose ◽  
Time Window ◽  
Critical Time ◽  
Grape Pomace ◽  
Delayed Treatment ◽  
Insulin Tolerance ◽  
Ovx Rats

Background: Estrogen (E2) loss is associated with insulin resistance. Natural compounds such as resveratrol (RESV) have potential insulin sensitizing effects. Grape pomace powder (GP) also contains RESV and other antioxidants. However, the ability of realistic, attainable concentrations of RESV and GP to reverse glucose intolerance in E2 deficient rats has not yet been explored.Purpose: The aim of the current study was to determine whether RESV and GP, in realistic amounts that could be achieved with supplementation, would be effective in restoring glucose tolerance in the ovariectomized (OVX) rat. Furthermore, there appears to be a critical time window following the loss of E2 when hormonal replacement is effective, with delayed treatment being ineffective and potentially detrimental. Therefore, we were particularly interested in examining the effectiveness of RESV and GP as a delayed treatment i.e. after the establishment of glucose intolerance, rather than administering at the onset of E2 loss. Results: In the present study, rats demonstrated impaired glucose tolerance, as determined by an intraperitoneal glucose tolerance test, 12 weeks after bilateral ovary removal. Subsequently, OVX animals were randomly placed into a sham or one of 3 treatment groups. The treatments were either i) a physiological oral dose of E2 (28µg/kg body mass), ii) RESV (5mg/kg body mass), or iii) GP (1.5g/100g of diet) for another 6 weeks. OVX animals were significantly heavier than non-OVX rats at the onset of glucose intolerance and this did not change throughout the treatment. None of the treatments restored glucose tolerance within the 6 weeks. Insulin tolerance did not worsen in OVX rats and was unaffected by treatment. Adipocyte size was generally increased in OVX animals and was not decreased with treatment.Conclusions: In conclusion, delayed E2, RESV and GP treatment do not restore glucose tolerance in OVX rats. Low dose RESV and GP supplementation may not be effective alternatives to HRT to restore compromised glucose tolerance.         Keywords: ovariectomy, estrogen, resveratrol, grape pomace, glucose tolerance, insulin tolerance, delayed treatment

P704Nanoliposomal anti-PCSK9 vaccine ameliorates glucose intolerance and insulin resistance in diabetic rats

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A A Momtazi-Borojeni ◽  
M R Jaafari ◽  
E Abdollahi ◽  
M Banach ◽  
A Sahebkar
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Tolerance Test ◽  
Diabetic Rats ◽  
Pcsk9 Inhibitors ◽  
Insulin Tolerance ◽  
Pcsk9 Inhibition ◽  
Histopathology Examination

Abstract Background PCSK9 inhibitors have emerged as an effective lipid-lowering approach. Although the results of available studies suggest a positive association of plasma PCSK9 levels with glycemic parameters and risk of DM, the effects of PCSK9 inhibitors on glucose intolerance and insulin resistance as the key features of DM remain unclear. Purpose The present study was directed to determine effect of vaccine-mediated PCSK9 inhibition on glucose intolerance and insulin resistance in experimental diabetic rats. Methods Nanoliposomal vaccine composing from PCSK9-linked nanoliposome particles mixed in Alum adjuvant was subcutaneously injected four times with bi-weekly intervals in Wistar-Albino rats. Two weeks after the last immunization, vaccinated and non-vaccinated rats were subjected to diabetes experiment induced by single intraperitoneal injection of streptozotocin (STZ). One week after STZ injection, glucose tolerance ability of each animal was evaluated by using oral glucose tolerance test (OGTT) on the overnight fasted rats with glucose dose at 2 g/kg. Two weeks after STZ injection, insulin tolerance test (ITT) viaintraperitoneal injection of insulin (0.8 U/kg) was performed to determine the measure of peripheral utilization of glucose. The plasma concentrations of total cholesterol (TC), LDL-C, HDL-C, and TG were measured. Results Nanoliposomal vaccine exposing PCSK9 peptide was found to provoke high-titers IgG antibody response against PCSK9 in rats, which was associated with the decrease plasma levels and function of plasma PCSK9. During the first week after STZ injection, it was indicated that the fasting blood glucose (FBG) level was 49% (−171.7±35 mg/dL, p<0.0001) lower in the vaccinated diabetic (VD) rats, when compared to the diabetic control (DC) rats. OGTT assessment revealed that the VS rats had significantly improved glucose tolerance ability and recorded significant reduction in the level of blood glucose over the period of 180 min, when compared with the DC rats. Measurement of integrated areas under the glucose curve values demonstrated that blood glucose levels were significantly (p<0.0001) decreased by 34.5% in the VS rats than the DC rats. In addition, ITT analysis showed that after insulin administration blood glucose level was decreased by 49.3% in the VS group compared with the DC group. The VS rats showed significantly lower (−26.65%, p=0.02) plasma LDL-C levels than the DC rats (Figure). Histopathology examination indicated that the pancreatic islet of the VS rats had a slightly decreased population of β-cells and few α-cells. Histopathology examination of the liver tissues of both VS and DC rats exhibited the normal histology with the normal hepatic architecture composed of hepatic lobules with normal central vein. Conclusions PCSK9 inhibition using liposomal vaccine can protect from glucose and insulin tolerance impairments in diabetic rats through an unknown and pancreatic-independent mechanism.

Maternal viral mimetic administration at the beginning of fetal hypothalamic nuclei development accelerates puberty in female rat offspring

2018 ◽  
Vol 96 (5) ◽  
pp. 506-514 ◽  
Author(s):  
Pinar Cakan ◽  
Sedat Yildiz ◽  
Tuba Ozgocer ◽  
Azibe Yildiz ◽  
Nigar Vardi
Keyword(s):  
Viral Infection ◽  
Body Mass ◽  
Time Window ◽  
Critical Time ◽  
Female Offspring ◽  
Poly I:C ◽  
Female Rat ◽  
Pregnant Rats ◽  
Rat Offspring ◽  
Polycytidylic Acid

This study aimed to investigate the effects of maternal viral infection during a critical time window of fetal hypothalamic development on timing of puberty in the female offspring. For that purpose, a viral mimetic (i.e., synthetic double-strand RNA, namely, polyinosinic–polycytidylic acid, poly (I:C)) or saline was injected (i.p.) to the pregnant rats during the beginning (day 12 of pregnancy, n = 5 for each group) or at the end of this time window (day 14 of pregnancy, n = 5 for each group). Four study groups were formed from the female pups (n = 9–10 pups/group). Following weaning of pups, vaginal opening and vaginal smearing was studied daily until 2 sequential estrous cycles were observed. During the second diestrus phase, blood samples were taken for progesterone, leptin, corticosterone, follicle-stimulating hormone, and luteinizing hormone. Maternal poly (I:C) injection on day 12 of pregnancy increased body mass and reduced the time to puberty in the female offspring. Neither poly (I:C) nor timing of injection affected other parameters studied (p > 0.05). It has been shown for the first time that maternal viral infection during the beginning of fetal hypothalamic development might hasten puberty by increasing body mass in rat offspring.

scholarly journals Effect of atorvastatin and rosuvastatin on glucose intolerance in low dose streptozotocin induced hyperglycemic Albino rats

2017 ◽  
Vol 6 (7) ◽  
pp. 1747
Author(s):  
Manju Gari ◽  
Abhishek Kumar ◽  
Lakhan Majhee
Keyword(s):  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Low Dose ◽  
Tolerance Test ◽  
Control Group ◽  
Albino Rats ◽  
Oral Glucose ◽  
Drug Of Choice ◽  
Patients At Risk ◽  
Group 2

Background: Dyslipidemia and glucose intolerance are closely associated with each other especially as a part of metabolic syndrome. Statins are the drug of choice for treatment of dyslipidemia and for primary prevention of coronary heart disease in diabetics. Recent studies indicate risk of new onset diabetes in patients receiving statins. Hence it was worthwhile to study the effect of two most commonly used statins, which differ in their lipophilicity, on glucose tolerance in prediabetic animal model.Methods: The study consisted of 3 groups with 6 wistar rats in each and hyperglycemia was induced by intraperitoneal injection of low dose (25mg/kg) streptozotocin. Group 1 served as control, group 2 and 3 were given Atorvastatin and Rosuvastatin respectively for 8 weeks. Oral glucose tolerance test (OGTT) was performed at 0,1 and 2 hrs after glucose load on days 0, 14, 28, 42 and 56 days.Results: Starting from 28th day onwards both the treatment groups showed progressive worsening of glucose tolerance throughout the study period in comparison to the control. The impairing effect on glucose tolerance was less pronounced in Rosuvastatin group as compared to Atorvastatin.Conclusions: Hydrophilic Rosuvastatin showing less impairing effect on glucose tolerance can be a rational choice than lipophilic Atorvastatin for prevention and control of dyslipidemia in patients at risk of developing frank diabetes or having impaired glucose tolerance.

scholarly journals Aspartame intake is associated with greater glucose intolerance in individuals with obesity

2016 ◽  
Vol 41 (7) ◽  
pp. 795-798 ◽  
Author(s):  
Jennifer L. Kuk ◽  
Ruth E. Brown
Keyword(s):  
Body Mass Index ◽  
Glucose Tolerance ◽  
Body Mass ◽  
Glucose Intolerance ◽  
Positive Association ◽  
Nhanes Iii

This study examined whether sucrose, fructose, aspartame, and saccharin influences the association between obesity and glucose tolerance in 2856 adults from the NHANES III survey. Aspartame intake significantly influenced the association between body mass index (BMI) and glucose tolerance (interaction: P = 0.004), wherein only those reporting aspartame intake had a steeper positive association between BMI and glucose tolerance than those reporting no aspartame intake. Therefore, consumption of aspartame is associated with greater obesity-related impairments in glucose tolerance.

scholarly journals Methionine restriction plus overload improves skeletal muscle and metabolic health in old mice on a high fat diet

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anandini Swaminathan ◽  
Andrej Fokin ◽  
Tomas Venckūnas ◽  
Hans Degens
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Muscle Mass ◽  
Body Mass ◽  
High Fat Diet ◽  
Control Diet ◽  
Metabolic Health ◽  
High Fat ◽  
Methionine Restriction ◽  
Old Mice

AbstractMethionine restriction (MR) has been shown to reduce the age-induced inflammation. We examined the effect of MR (0.17% methionine, 10% kCal fat) and MR + high fat diet (HFD) (0.17% methionine, 45% kCal fat) on body mass, food intake, glucose tolerance, resting energy expenditure, hind limb muscle mass, denervation-induced atrophy and overload-induced hypertrophy in young and old mice. In old mice, MR and MR + HFD induced a decrease in body mass. Muscle mass per body mass was lower in old compared to young mice. MR restored some of the HFD-induced reduction in muscle oxidative capacity. The denervation-induced atrophy of the m. gastrocnemius was larger in animals on MR than on a control diet, irrespective of age. Old mice on MR had larger hypertrophy of m. plantaris. Irrespective of age, MR and MR + HFD had better glucose tolerance compared to the other groups. Young and old mice on MR + HFD had a higher resting VO2 per body mass than HFD group. Mice on MR and MR + HFD had a resting respiratory quotient closer to 0.70, irrespective of age, indicating an increased utilization of lipids. In conclusion, MR in combination with resistance training may improve skeletal muscle and metabolic health in old age even in the face of obesity.

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.

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