scholarly journals Chronic exposure to low doses of lipopolysaccharide and high-fat feeding increases body mass without affecting glucose tolerance in female rats

2015 ◽  
Vol 3 (11) ◽  
pp. e12584 ◽  
Author(s):  
Anete Dudele ◽  
Christina W. Fischer ◽  
Betina Elfving ◽  
Gregers Wegener ◽  
Tobias Wang ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Body Mass ◽  
Chronic Exposure ◽  
Female Rats ◽  
Low Doses ◽  
High Fat ◽  
Fat Feeding

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.

Antecedent protein restriction exacerbates development of impaired insulin action after high-fat feeding

1999 ◽  
Vol 276 (1) ◽  
pp. E85-E93 ◽  
Author(s):  
Mark J. Holness ◽  
Mary C. Sugden
Keyword(s):  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Insulin Action ◽  
Protein Restriction ◽  
Protein Diet ◽  
Glucose Disposal ◽  
High Fat ◽  
Impaired Insulin ◽  
Impaired Insulin Action ◽  
Fat Feeding

The study investigated whether a persistent impairment of insulin secretion resulting from mild protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of the diabetogenic challenge of high-fat feeding. Offspring of dams provided with either control (20% protein) diet (C) or an isocaloric restricted (8%) protein diet (PR) were weaned onto the maintenance diet with which their mothers had been provided. At 20 wk of age, protein restriction enhanced glucose tolerance despite impaired insulin secretion and an augmented and sensitized lipolytic response to norepinephrine in adipocytes. C and PR rats were then transferred to a high-fat diet (HF, 19% protein, 22% lipid, 34% carbohydrate) and sampled after 8 wk. These groups are termed C-HF and PR-HF. Glucose tolerance was impaired in PR-HF, but not C-HF, rats. Insulin-stimulated glucose disposal rates were significantly lower (by 30%; P < 0.01) in the PR-HF group than in the C-HF group, and a specific impairment of antilipolytic response of insulin was unmasked in adipocytes from PR-HF, but not C-HF, rats. The study demonstrates that antecedent protein restriction accelerates and augments the development of impaired glucoregulation and insulin resistance after high-fat feeding.

EFFECTS OF ORAL CONTRACEPTIVES AND THEIR COMPONENTS ON GLUCOSE TOLERANCE IN RATS

1969 ◽  
Vol 62 (3) ◽  
pp. 438-448 ◽  
Author(s):  
R. L. Fenichel ◽  
R. M. Purse ◽  
H. E. Alburn ◽  
R. A. Edgren
Keyword(s):  
Glucose Tolerance ◽  
High Protein Diet ◽  
Female Rats ◽  
High Fat ◽  
Intact Female ◽  
Control Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Human Dose ◽  
Glucose Tolerance Tests

ABSTRACT Treatment of adult female spayed rats with norgestrel, ethynyl oestradiol and their combination (Ovral®) at doses approximating 1 and 25 fold multiples of the human dose protected them against the combined diabetogenic influence of a glucose load and the hyperglycaemic effect of reduced insulin B-chain. Norgestrel and Ovral® appeared to be antidiabetogenic since they reversed the B-chain-induced hyperglycaemia. Various steroidal contraceptives and certain of their components failed to modify B-chain-induced hyperglycaemia in spayed rats sensitized with a high fat, high protein diet. Normal intact female rats treated with norgestrel, ethynyl oestradiol and their combinations and given glucose tolerance tests produced glucose responses higher than those of controls, but since these groups showed recovery to or toward control blood glucose levels, insulin mobilization was apparently normal. In a second experiment, Ovral® and various contraceptive formulations failed to produce significant alterations in glucose tolerance. None of these studies suggested a diabetogenic effect of the contraceptive steroids employed; in fact, the first study with reduced insulin B-chain suggested an anti-diabetogenic effect for Ovral®.

scholarly journals APP deficiency results in resistance to obesity but impairs glucose tolerance upon high fat feeding

2018 ◽  
Vol 237 (3) ◽  
pp. 311-322 ◽  
Author(s):  
Juliane K Czeczor ◽  
Amanda J Genders ◽  
Kathryn Aston-Mourney ◽  
Timothy Connor ◽  
Liam G Hall ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Glucose Tolerance ◽  
Cell Mass ◽  
Tolerance Test ◽  
Whole Body ◽  
Dark Phase ◽  
High Fat ◽  
Neuronal Metabolism ◽  
Fat Feeding ◽  
Deficient Mice

The amyloid precursor protein (APP) generates a number of peptides when processed through different cleavage mechanisms, including the amyloid beta peptide that is implicated in the development of Alzheimer’s disease. It is well established that APP via its cleaved peptides regulates aspects of neuronal metabolism. Emerging evidence suggests that amyloidogenic processing of APP can lead to altered systemic metabolism, similar to that observed in metabolic disease states. In the present study, we investigated the effect of APP deficiency on obesity-induced alterations in systemic metabolism. Compared with WT littermates, APP-deficient mice were resistant to diet-induced obesity, which was linked to higher energy expenditure and lipid oxidation throughout the dark phase and was associated with increased spontaneous physical activity. Consistent with this lean phenotype, APP-deficient mice fed a high-fat diet (HFD) had normal insulin tolerance. However, despite normal insulin action, these mice were glucose intolerant, similar to WT mice fed a HFD. This was associated with reduced plasma insulin in the early phase of the glucose tolerance test. Analysis of the pancreas showed that APP was required to maintain normal islet and β-cell mass under high fat feeding conditions. These studies show that, in addition to regulating aspects of neuronal metabolism, APP is an important regulator of whole body energy expenditure and glucose homeostasis under high fat feeding conditions.

scholarly journals Sex-dependent hepatic transcripts and metabolites in the development of glucose intolerance and insulin resistance in Zucker diabetic fatty rats

2011 ◽  
Vol 47 (2) ◽  
pp. 129-143 ◽  
Author(s):  
Carolina Gustavsson ◽  
Tomoyoshi Soga ◽  
Erik Wahlström ◽  
Mattias Vesterlund ◽  
Alireza Azimi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Stress Responses ◽  
Female Rats ◽  
Male Rats ◽  
High Fat ◽  
Prediabetic State ◽  
Flight Mass Spectrometry ◽  
Zucker Diabetic Fatty Rats

Male Zucker diabetic fatty (mZDF) rats spontaneously develop type 2 diabetes, whereas females only become diabetic when fed a diabetogenic high-fat diet (high-fat-fed female ZDF rat, HF-fZDF). The aim of this study was to investigate if differences in liver functions could provide clues to this sex difference. Non-diabetic obese fZDF rats were compared with either mZDF or HF-fZDF regarding hepatic molecular profiles, to single out those components that might be protective in the females. High-fat feeding in fZDF led to enhanced weight gain, increased blood glucose and insulin levels, reduced insulin sensitivity and a trend towards reduced glucose tolerance, indicative of a prediabetic state. mZDF rats were diabetic, with low levels of insulin, high levels of glucose, reduced insulin sensitivity and impaired glucose tolerance. Transcript profiling and capillary electrophoresis time-of-flight mass spectrometry were used to indentify hepatic transcripts and metabolites that might be related to this. Many diet-induced alterations in transcript and metabolite levels in female rats were towards a ‘male-like’ phenotype, including reduced lipogenesis, increased fatty acid (FA) oxidation and increased oxidative stress responses. Alterations detected at the level of hepatic metabolites, indicated lower capacity for glutathione (GSH) production in male rats, and higher GSH turnover in females. Taken together, this could be interpreted as if anabolic pathways involving lipogenesis and lipid output might limit the degree of FA oxidation and oxidative stress in female rats. Together with a greater capacity to produce GSH, these hepatic sex differences might contribute to the sex-different development of diabetes in ZDF rats.

scholarly journals Chronic exposure to low doses of estradiol-17ß increases blood pressure in young female rats: A possible role for central Endothelin-1

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Madhan Subramanian ◽  
Sheba M. J. MohanKumar ◽  
Priya Balasubramanian ◽  
Carrie A. Northcott ◽  
Hannah Garver ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Exposure ◽  
Young Female ◽  
Female Rats ◽  
Low Doses ◽  
Endothelin 1

Chronic high fat feeding increases anxiety-like behaviour and reduces transcript abundance of glucocorticoid signalling genes in the hippocampus of female rats

2015 ◽  
Vol 286 ◽  
pp. 265-270 ◽  
Author(s):  
Shathveekan Sivanathan ◽  
Kabriya Thavartnam ◽  
Shahneen Arif ◽  
Trisha Elegino ◽  
Patrick O. McGowan
Keyword(s):  
Transcript Abundance ◽  
Female Rats ◽  
High Fat ◽  
Fat Feeding

Adult Consequences of Post-weaning High Fat Feeding on the Limbic–HPA Axis of Female Rats

2009 ◽  
Vol 30 (4) ◽  
pp. 521-530 ◽  
Author(s):  
George Boukouvalas ◽  
Kyriaki Gerozissis ◽  
Efthimia Kitraki
Keyword(s):  
Hpa Axis ◽  
Female Rats ◽  
High Fat ◽  
Fat Feeding

scholarly journals Hypothalamic JNK1 and IKKβ Activation and Impaired Early Postnatal Glucose Metabolism after Maternal Perinatal High-Fat Feeding

Endocrinology ◽  
2012 ◽  
Vol 153 (2) ◽  
pp. 770-781 ◽  
Author(s):  
Eva Rother ◽  
Ruth Kuschewski ◽  
Miguel Angel Alejandre Alcazar ◽  
André Oberthuer ◽  
Inga Bae-Gartz ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Saturated Fatty Acids ◽  
Sympathetic Innervation ◽  
Virgin Female ◽  
High Fat ◽  
Hepatic Expression ◽  
Iκb Kinase ◽  
Hypothalamic Inflammation ◽  
Fat Feeding

Hypothalamic inflammation has been demonstrated to be an important mechanism in the pathogenesis of obesity-induced type 2 diabetes mellitus. Feeding pregnant and lactating rodents a diet rich in saturated fatty acids has consistently been shown to predispose the offspring for the development of obesity and impaired glucose metabolism. However, hypothalamic inflammation in the offspring has not been addressed as a potential underlying mechanism. In this study, virgin female C57BL/6 mice received high-fat feeding starting at conception until weaning of the offspring at postnatal d 21. The offspring developed increased body weight, body fat content, and serum leptin concentrations during the nursing period. Analysis of hypothalamic tissue of the offspring at postnatal d 21 showed up-regulation of several members of the toll-like receptor 4 signaling cascade and subsequent activation of c-Jun N-terminal kinase 1 and IκB kinase-β inflammatory pathways. Interestingly, glucose tolerance testing in the offspring revealed signs of impaired glucose tolerance along with increased hepatic expression of the key gluconeogenic enzyme phosphoenolpyruvate carboxykinase. In addition, significantly increased hepatic and pancreatic PGC1α expression suggests a role for sympathetic innervation in mediating the effects of hypothalamic inflammation to the periphery. Taken together, our data indicate an important role for hypothalamic inflammation in the early pathogenesis of glucose intolerance after maternal perinatal high-fat feeding.

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