A four-week high fat diet does not alter plasma glucose or metabolic physiology in wild-caught mourning doves (Zenaida macroura)

Previous studies demonstrate that the addition of naringenin, a grapefruit flavonoid, to a high-fat diet prevents the development of many disorders of the metabolic syndrome and atherosclerosis in Ldlr-/- mice. Furthermore, in intervention studies, the addition of naringenin to a high-fat, high cholesterol (HFHC) diet reversed pre-established obesity, hyperlipidemia, hepatic steatosis, insulin resistance and improved atherosclerotic lesion pathology, but not lesion size. In the present intervention study, we tested the hypothesis that addition of naringenin to a chow diet would further improve pre-established metabolic dysregulation and attenuate lesion development, compared to chow alone. Ldlr-/- mice were fed a HFHC diet for 12 weeks to induce metabolic dysregulation. Subsequently, mice received one of 3 diets for another 12 weeks: 1) continuation of the HFHC diet, 2) an isoflavone-free chow diet or 3) isoflavone-free chow with 3% naringenin. At 12 weeks, the HFHC diet induced significant weight gain and increased adiposity. Intervention with chow alone reduced the weight gained during induction by 22%, whereas the addition of naringenin to chow induced a weight loss of 71%. Specifically, the reduction in adiposity was 2.75-times greater in naringenin-treated mice, compared to chow alone. The HFHC diet increased VLDL cholesterol 20-fold and LDL cholesterol 5-fold, which were reduced by intervention with both chow (>60%) and chow supplemented with naringenin (>80%). The HFHC diet induced insulin resistance and glucose intolerance. Naringenin improved insulin tolerance (plasma glucose AUC -38%) and glucose tolerance (plasma glucose AUC -58%), which was accompanied by normalization of plasma insulin and glucose. HFHC-induction promoted the development of intermediate atherosclerotic lesions. Continuation of the HFHC diet doubled lesion size. Intervention with chow alone attenuated lesion size progression by 65%. The addition of naringenin to chow slowed lesion progression by 90%, resulting in smaller lesions compared to chow intervention alone (P=0.042). We conclude that intervention with naringenin-supplemented chow enhances weight loss, improves metabolic dysregulation and halts the progression of atherosclerosis.

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

British Journal Of Nutrition ◽

10.1079/bjn19880046 ◽

1988 ◽

Vol 59 (3) ◽

pp. 373-380 ◽

Cited By ~ 40

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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THE EFFECT OF A HIGH-FAT DIET ON GLUCOSE, INSULIN SENSITIVITY AND PLASMA INSULIN IN RATS

Journal of Endocrinology ◽

10.1677/joe.0.0420489 ◽

1968 ◽

Vol 42 (4) ◽

pp. 489-494 ◽

Cited By ~ 37

Author(s):

E. BLÁZQUEZ ◽

C. LOPEZ QUIJADA

Keyword(s):

Plasma Glucose ◽

High Fat Diet ◽

Plasma Insulin ◽

Diet Group ◽

Insulin Concentration ◽

Control Group ◽

High Fat ◽

Plasma Insulin Concentration ◽

The Mean

SUMMARY The influence of the diet on the levels of insulin was studied in rats on a high-fat diet. Plasma and glucose insulin concentrations of a control group and of rats on a high-fat diet were compared, and so was the insulin concentration in the pancreas of the two groups. The mean plasma insulin concentration in the control group was 40 μ-u./ml. and that of insulin extracted from the pancreas was 2·5 μg./100 mg. tissue; plasma glucose was 156 mg./100 ml. The animals fed on a high-fat diet showed diabetic features. The mean plasma insulin level was 9 μ-u./ml., and plasma glucose increased to 210 mg./100 ml. The insulin concentration in the pancreas was not significantly different from that in the controls. In vitro the epididymal fat and the diaphragm of the high-fat-diet group were less sensitive to insulin than the same tissues in the control group.

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Effect of resveratrol on diabetic neuropathy in wistar albino rats

International Journal of Basic & Clinical Pharmacology ◽

10.18203/2319-2003.ijbcp20195635 ◽

2019 ◽

Vol 9 (1) ◽

pp. 16

Author(s):

Smita Das ◽

Jayanti Prava Behera ◽

Y. Rojaramani ◽

Rashmi Ranjan Mohanty

Keyword(s):

Diabetic Neuropathy ◽

Lipid Profile ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

High Fat Diet ◽

Albino Rats ◽

High Fat ◽

Multiple Comparison Test ◽

Wistar Albino Rats

Background: Type 2 diabetes mellitus (DM) is a common chronic disease with increasing prevalence worldwide. Prolonged uncontrolled hyperglycemia, dyslipidemia are major risk factor for its complication like neuropathy. Since there is no definite treatment for diabetic neuropathy, this study aims to evaluate the effect of resveratrol on diabetic neuropathy in high fat diet with low dose streptozotocin induced type-2 DM model in wistar albino rats.Methods: First type 2 diabetic rat model was established. Wistar albino rats, fed with high-fat diet (HFD) rendered diabetic with streptozotocin, were divided into 6 groups, disease control (DC) treated with vehicle, standard control (SC) which received metformin, test groups treated with 5, 10, and 20 mg/kg b.w. of resveratrol and combination of half dose of metformin and resveratrol (10 mg/kg) (TC). A group of six normal animals served as normal control (NC), another six as HFD control. Fasting plasma glucose, lipid profile were measured one week after induction of diabetes. The animals were then treated orally for 2 weeks after which the same parameters were repeated. Behavioral biomarkers for neuropathy are measured in 4 weeks and 6 weeks of treatment. The in-vivo results were analyzed by one way ANOVA followed by Tukey’s multiple comparison test for biochemical parameters and Kruskal Wallis test followed by Dun’s multiple comparison test for behavioral biomarkers.Results: Increase in fasting plasma glucose (FPG), deranged lipid profile, increased neuropathy in DC compared to NC, HFD control while a significant decrease in FBG, improved pain behavior with SC, test groups (p<0.05) as compared to the DC group.Conclusions: Resveratrol prevents diabetic neuropathy.

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Loss of ARC worsens high fat diet-induced hyperglycemia in mice

Journal of Endocrinology ◽

10.1530/joe-20-0612 ◽

2021 ◽

Author(s):

Andrew T Templin ◽

Christine Schmidt ◽

Meghan F Hogan ◽

Nathalie Esser ◽

Richard N Kitsis ◽

...

Keyword(s):

Cell Death ◽

Body Weight ◽

Plasma Glucose ◽

Fasting Plasma Glucose ◽

High Fat Diet ◽

Metabolic Adaptation ◽

High Fat ◽

Β Cell ◽

Fasting Plasma

Apoptosis repressor with caspase recruitment domain (ARC) is an endogenous inhibitor of cell death signaling that is expressed in insulin-producing β-cells. ARC has been shown to reduce β-cell death in response to diabetogenic stimuli in vitro, but its role in maintaining glucose homeostasis in vivo has not been fully established. Here we examined whether loss of ARC in FVB background mice exacerbates high fat diet (HFD)-induced hyperglycemia in vivo over 24 weeks. Prior to commencing 24-week HFD, ARC-/- mice had lower body weight than wild type (WT) mice. This body weight difference was maintained until the end of the study and was associated with decreased epididymal and inguinal adipose tissue mass in ARC-/- mice. Non-fasting plasma glucose was not different between ARC-/- and WT mice prior to HFD feeding, and ARC-/- mice displayed a greater increase in plasma glucose over the first 4 weeks of HFD. Plasma glucose remained elevated in ARC-/- mice after 16 weeks of HFD feeding, at which time it had returned to baseline in WT mice. Following 24 weeks of HFD, non-fasting plasma glucose in ARC-/- mice returned to baseline and was not different from WT mice. At this final time point, no differences in plasma glucose or insulin were observed under fasted conditions or following IV glucose administration between genotypes. However, HFD-fed ARC-/- mice exhibited significantly decreased β-cell area compared to WT mice. Thus, ARC deficiency delays, but does not prevent, metabolic adaptation to HFD feeding in mice, worsening transient HFD-induced hyperglycemia.

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The effect of Plant by-products on liver functions and plasma glucose in rats fed a high fat diet induced obesity.

مجلة کلیة التربیة. بورسعید ◽

10.21608/jftp.2016.36796 ◽

2016 ◽

Vol 19 (19) ◽

pp. 551-561

Author(s):

سارة أحمد محمد السید أحمد

Keyword(s):

Plasma Glucose ◽

High Fat Diet ◽

High Fat ◽

Diet Induced Obesity ◽

Liver Functions ◽

By Products

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Effect of Bergenin on the Kidney of C57BL/6J Mice with High Fat-Diet Induced Oxidative Stress

International Letters of Natural Sciences ◽

10.18052/www.scipress.com/ilns.54.58 ◽

2016 ◽

Vol 54 ◽

pp. 58-65 ◽

Cited By ~ 1

Author(s):

Sagadevan Ambika ◽

Ramalingam Saravanan

Keyword(s):

Lipid Peroxidation ◽

Plasma Glucose ◽

High Fat Diet ◽

Histopathological Examination ◽

Intragastric Administration ◽

Standard Diet ◽

Lipid Peroxidation Product ◽

High Fat ◽

Standard Drug ◽

Peroxidation Product

The present study evaluated the protective effect of bergenin on high fat diet (HFD) induced diabetic mice. C57BL/6J mice were segregated in two groups, one fed standard diet (NC) and the other fed HFD for 16 weeks. Mice were fed continuously with high fat diet for 16 weeks and subjected to intragastric administration of bergenin (10, 20 and 40 mg/kg body weight (BW)), metformin (25 mg/kg BW) 9 to 16 weeks. At the end of the treatment nephritic markers, lipid peroxidation product, antioxidant and histopathological examination were carried out to assess the efficacy of the treatment. HFD fed mice showed increased plasma glucose, insulin, altered nephritic markers, antioxidant and histopathological abnormalities. Oral Treatment with bergenin (40 mg/kg BW) showed near normalized levels of plasma glucose, lipid peroxidation product, antioxidants, improved insulin and reduced kidney damage. The effects of bergenin were comparable with standard drug, metformin. These data suggest that bergenin protect kidney from deleterious effect of glucose.

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Sub-chronic administration of the 11β-HSD1 inhibitor, carbenoxolone, improves glucose tolerance and insulin sensitivity in mice with diet-induced obesity

Biological Chemistry ◽

10.1515/bc.2008.049 ◽

2008 ◽

Vol 389 (4) ◽

pp. 441-445 ◽

Cited By ~ 19

Author(s):

Ashley Taylor ◽

Nigel Irwin ◽

Aine M. McKillop ◽

Peter R. Flatt ◽

Victor A. Gault

Keyword(s):

Gene Expression ◽

Body Weight ◽

Plasma Glucose ◽

High Fat Diet ◽

Receptor Gene ◽

Daily Administration ◽

Metabolic Effects ◽

High Fat ◽

Diet Induced Obesity ◽

Glucocorticoid Receptor Gene

Abstract We have examined the metabolic effects of daily administration of carbenoxolone (CBX), a naturally occurring 11β-hydroxysteroid dehydrogenase (11β-HSD1) inhibitor, in mice with high fat diet-induced insulin resistance and obesity. Eight-week-old male Swiss TO mice placed on a synthetic high fat diet received daily intraperitoneal injections of either saline vehicle or CBX over a 16-day period. Daily administration of CBX had no effect on food intake, but significantly lowered body weight (1.1- to 1.2-fold) compared to saline-treated controls. Non-fasting plasma glucose levels were significantly decreased (1.6-fold) by CBX treatment on day 4 and remained lower throughout the treatment period. Circulating plasma corticosterone levels were not significantly altered by CBX treatment. Plasma glucose concentrations of CBX-treated mice were significantly reduced (1.4-fold) following an intraperitoneal glucose load compared with saline controls. Similarly, after 16-day treatment with CBX, exogenous insulin evoked a significantly greater reduction in glucose concentrations (1.4- to 1.8-fold). 11β-HSD1 gene expression was significantly down-regulated in liver, whereas glucocorticoid receptor gene expression was increased in both liver and adipose tissue following CBX treatment. The reduced body weight and improved metabolic control in mice with high fat diet-induced obesity upon daily CBX administration highlights the potential value of selective 11β-HSD1 inhibition as a new route for the treatment of type 2 diabetes and obesity.

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