scholarly journals Differential Effects of Short-term Ketogenic, High Fat and Fructose-enriched Diets on Metabolic Parameters in Mice (P08-042-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Natalia Cortez ◽  
John Solitro ◽  
Brian Hong ◽  
Emily Villarreal ◽  
Gerardo Mackenzie
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Grip Strength ◽  
Glucose Homeostasis ◽  
Control Diet ◽  
Oral Glucose ◽  
High Fat ◽  
Carbohydrate Source ◽  
Strength Performance ◽  
Glucose Levels

Abstract Objectives Dietary composition influences multiple facets of human health and is inextricably linked to chronic metabolic conditions such as obesity, type 2 diabetes, cardiovascular disease and cancer. Thus, the objective of this study was to evaluate the effects of a ketogenic (KD), a high fat (HF), and a fructose-enriched (FR) diets on glucose homeostasis, body composition and grip strength performance in mice. Methods Healthy C57BL/6 J mice (5–6 mice/group) were fed, either a control diet containing approximately 16% total calories from fat (CT), a diet containing 89% fat (KD), a diet with 50% total calories from fat (HF), or a diet with 32% fructose as carbohydrate source (FR). All diets contained 10% protein and all mice were fed ad libitum for 8 weeks. At baseline and 8 weeks, we evaluated body composition using NMR relaxometry, grip strength, non-fasting glucose levels, and ketone levels. In addition, oral glucose tolerance test (OGTT) was conducted by administering glucose by oral gavage (1 g/kg body weight) after 15 hour-fasting and blood glucose levels were measured at 0, 30, 60, 90, and 120 min after glucose administration. Results All mice, irrespectively of their experimental diet groups, increased their body weight, fat mass and adiposity without significant differences among them. After 4 weeks, the HF (P < 0.05) and FR (P < 0.01) groups had significantly higher glucose levels than control. At 8 weeks, the KD groups showed an improved glucose homeostasis compared to CT group, as determined by OGTT. Moreover, compared to the CT group, grip strength performance increased (although did not reached significance) in the KD group (P = 0.054), and decreased in the FR group (P < 0.05). Moreover, when compared to their respective baseline values, grip strength performance increased in KD-fed mice and decreased in FR-fed mice, but differences among them were not statistically significant (P = 0.07). Conclusions Our preliminary findings indicate that altering macronutrient composition can lead to metabolic and physiological changes. Among the three diets tested, the KD showed an improved glucose utilization and better grip strength performance in mice. Additional mechanistic studies are warranted to better understand these metabolic differences among the experimental diets. Funding Sources funds from the University of California, Davis.

scholarly journals High fat-fed GPR55 null mice display impaired glucose tolerance without concomitant changes in energy balance or insulin sensitivity but are less responsive to the effects of the cannabinoids rimonabant or Δ(9)-tetrahydrocannabivarin on weight gain

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9811
Author(s):  
Edward T. Wargent ◽  
Malgorzata Kepczynska ◽  
Mohamed Sghaier Zaibi ◽  
David C. Hislop ◽  
Jonathan R.S. Arch ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Wild Type ◽  
High Fat ◽  
Insulin Tolerance

Background The insulin-sensitizing phytocannabinoid, Δ(9)-tetrahydrocannabivarin (THCV) can signal partly via G-protein coupled receptor-55 (GPR55 behaving as either an agonist or an antagonist depending on the assay). The cannabinoid receptor type 1 (CB1R) inverse agonist rimonabant is also a GPR55 agonist under some conditions. Previous studies have shown varied effects of deletion of GPR55 on energy balance and glucose homeostasis in mice. The contribution of signalling via GPR55 to the metabolic effects of THCV and rimonabant has been little studied. Methods In a preliminary experiment, energy balance and glucose homeostasis were studied in GPR55 knockout and wild-type mice fed on both standard chow (to 20 weeks of age) and high fat diets (from 6 to 15 weeks of age). In the main experiment, all mice were fed on the high fat diet (from 6 to 14 weeks of age). In addition to replicating the preliminary experiment, the effects of once daily administration of THCV (15 mg kg−1 po) and rimonabant (10 mg kg−1 po) were compared in the two genotypes. Results There was no effect of genotype on absolute body weight or weight gain, body composition measured by either dual-energy X-ray absorptiometry or Nuclear Magnetic Resonance (NMR), fat pad weights, food intake, energy expenditure, locomotor activity, glucose tolerance or insulin tolerance in mice fed on chow. When the mice were fed a high fat diet, there was again no effect of genotype on these various aspects of energy balance. However, in both experiments, glucose tolerance was worse in the knockout than the wild-type mice. Genotype did not affect insulin tolerance in either experiment. Weight loss in rimonabant- and THCV-treated mice was lower in knockout than in wild-type mice, but surprisingly there was no detectable effect of genotype on the effects of the drugs on any aspect of glucose homeostasis after taking into account the effect of genotype in vehicle-treated mice. Conclusions Our two experiments differ from those reported by others in finding impaired glucose tolerance in GPR55 knockout mice in the absence of any effect on body weight, body composition, locomotor activity or energy expenditure. Nor could we detect any effect of genotype on insulin tolerance, so the possibility that GPR55 regulates glucose-stimulated insulin secretion merits further investigation. By contrast with the genotype effect in untreated mice, we found that THCV and rimonabant reduced weight gain, and this effect was in part mediated by GPR55.

Improvement of mild hypoinsulinaemic diabetes in the rat by low non-toxic doses of vanadate

1994 ◽  
Vol 142 (3) ◽  
pp. 555-561 ◽  
Author(s):  
J C Henquin ◽  
F Carton ◽  
L N Ongemba ◽  
D J Becker
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Glucose Homeostasis ◽  
Plasma Glucose ◽  
Body Weight Gain ◽  
Oral Glucose ◽  
Low Doses ◽  
Glucose Levels ◽  
Vanadium Salts

Abstract To exert their anti-diabetic effects in animals with overt alterations of glucose homeostasis, vanadium salts must be administered in high doses, which also cause decreases in food intake and body weight gain. In this study, we evaluated the effect of low doses of vanadate in rats made mildly diabetic (fed plasma glucose levels ∼11 mmol/l) and moderately hypoinsulinaemic by the injection of streptozotocin 4 days after birth. Vanadate was added to food and drinking water, at concentrations that led to the consumption of about 1 mg vanadium element per day (∼2·65 mg vanadium/kg per day in adult rats), i.e. three to fivefold less than in previous studies. The treatment was started at weaning and lasted 22 weeks (V rats), or was administered for 9 weeks only from the age of 3 months (C-V rats). Food intake and body weight gain were not affected in V rats and decreased by no more than 10% in C-V rats. In V rats, fasted and fed plasma glucose levels were decreased by about 0·5 and 2–3 mmol/l, respectively. The rises in glycaemia after three oral glucose tolerance tests were also clearly attenuated. These effects were not accompanied by any changes in plasma insulin levels. Pancreatic insulin reserves (decreased by two-thirds as compared with normal rats) were not affected by the treatment. A decrease in plasma glucose levels was also noted in C-V rats, and this improvement disappeared upon cessation of the treatment. In conclusion, oral vanadate improves glucose homeostasis in rats with moderate insulin deficiency and diabetes, even when the element is administered at low doses which have practically no repercussions on food intake and body weight gain. This indicates that vanadium salts have genuine beneficial effects on glucose metabolism in vivo. Journal of Endocrinology (1994) 142, 555–561

scholarly journals Inactivation of the adrenergic receptor β2 disrupts glucose homeostasis in mice

2014 ◽  
Vol 221 (3) ◽  
pp. 381-390 ◽  
Author(s):  
Gustavo W Fernandes ◽  
Cintia B Ueta ◽  
Tatiane L Fonseca ◽  
Cecilia H A Gouveia ◽  
Carmen L Lancellotti ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Expenditure ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Liver Steatosis ◽  
Mrna Levels ◽  
High Fat ◽  
Adaptive Thermogenesis ◽  
Brown Adipose ◽  
Similar Body

Three types of beta adrenergic receptors (ARβ1–3) mediate the sympathetic activation of brown adipose tissue (BAT), the key thermogenic site for mice which is also present in adult humans. In this study, we evaluated adaptive thermogenesis and metabolic profile of a mouse withArβ2knockout (ARβ2KO). At room temperature, ARβ2KO mice have normal core temperature and, upon acute cold exposure (4 °C for 4 h), ARβ2KO mice accelerate energy expenditure normally and attempt to maintain body temperature. ARβ2KO mice also exhibited normal interscapular BAT thermal profiles during a 30-min infusion of norepinephrine or dobutamine, possibly due to marked elevation of interscapular BAT (iBAT) and ofArβ1, andArβ3mRNA levels. In addition, ARβ2KO mice exhibit similar body weight, adiposity, fasting plasma glucose, cholesterol, and triglycerides when compared with WT controls, but exhibit marked fasting hyperinsulinemia and elevation in hepaticPepck(Pck1) mRNA levels. The animals were fed a high-fat diet (40% fat) for 6 weeks, ARβ2KO mice doubled their caloric intake, accelerated energy expenditure, and inducedUcp1expression in a manner similar to WT controls, exhibiting a similar body weight gain and increase in the size of white adipocytes to the WT controls. However, ARβ2KO mice maintain fasting hyperglycemia as compared with WT controls despite very elevated insulin levels, but similar degrees of liver steatosis and hyperlipidemia. In conclusion, inactivation of the ARβ2KO pathway preserves cold- and diet-induced adaptive thermogenesis but disrupts glucose homeostasis possibly by accelerating hepatic glucose production and insulin secretion. Feeding on a high-fat diet worsens the metabolic imbalance, with significant fasting hyperglycemia but similar liver structure and lipid profile to the WT controls.

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

Abstract 58: Angiotensin-(1-7) Mas Receptors In The Arcuate Nucleus Of The Hypothalamus Protect Against High Fat Diet-induced Insulin Resistance In Female Mice

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Darren Mehay ◽  
Sarah Bingaman ◽  
Yuval Silberman ◽  
Amy Arnold
Keyword(s):  
Body Composition ◽  
Insulin Sensitivity ◽  
Energy Balance ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Metabolic Regulation ◽  
Arcuate Nucleus ◽  
Control Diet ◽  
High Fat ◽  
Metabolic Outcomes

Angiotensin (Ang)-(1-7) is a protective hormone of the renin-angiotensin system that improves insulin sensitivity, glucose tolerance, and energy balance in obese rodents. Our recent findings suggest that Ang-(1-7) activates mas receptors (MasR) in the arcuate nucleus of the hypothalamus (ARC), a brain region critical to control of energy balance and glucose homeostasis, to induce these positive metabolic effects. The distribution of MasR in the ARC and their role in metabolic regulation, however, is unknown. We hypothesized: (1) MasR are expressed in the ARC; and (2) deletion of ARC MasR leads to worsened metabolic outcomes following high fat diet (HFD). To test this, male and female C57Bl/6J mice were fed a 60% HFD or matched control diet ad libitum for 12 weeks. RNAscope in situ hybridization was performed on coronal ARC sections in rostral-middle-caudal regions to determine percentage of MasR positive neurons (n=5/group). In a second experiment, we assessed body composition and insulin and glucose tolerance in transgenic mice with deletion of MasR in ARC neurons (MasR-flox with AAV5-hsyn-GFP-Cre). RNAscope revealed a wide distribution on MasR-positive cells throughout the rostral to caudal extent of the ARC. The average percentage of MasR positive neurons was increased in females versus males, with HFD tending to increase MasR expression in both sexes (control diet male: 11±2; control diet female: 17±3; HFD male: 15±5; HFD female: 24±2; p sex : 0.030; p diet : 0.066; p int : 0.615; two-way ANOVA). Deletion of MasR in ARC neurons worsened insulin sensitivity in HFD but not control diet females (area under the curve for change in glucose from baseline: -1989±1359 HFD control virus vs. 2530±1762 HFD Cre virus; p=0.016), while fasting glucose, glucose tolerance, and body composition did not change. There was no effect of ARC MasR deletion on metabolic outcomes in control diet or HFD male mice. These findings suggest females have more MasR positive neurons in the ARC compared to males, which may be a sex-specific protective mechanism for glucose homeostasis. While further studies are needed to explore the role of ARC MasR in metabolic regulation, these findings support targeting Ang-(1-7) as an innovative strategy in obesity.

scholarly journals Tetrahydro iso-Alpha Acids from Hops Improve Glucose Homeostasis and Reduce Body Weight Gain and Metabolic Endotoxemia in High-Fat Diet-Fed Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e33858 ◽  
Author(s):  
Amandine Everard ◽  
Lucie Geurts ◽  
Marie Van Roye ◽  
Nathalie M. Delzenne ◽  
Patrice D. Cani
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Glucose Homeostasis ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Reduce Body Weight ◽  
Metabolic Endotoxemia

scholarly journals Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-α

2007 ◽  
Vol 97 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Nerea Pérez-Echarri ◽  
J. Alfredo Martínez ◽  
Amelia Marti ◽  
María J. Moreno-Aliaga
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Control Diet ◽  
Cafeteria Diet ◽  
High Fat ◽  
Beneficial Effects

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0·09), a decrease in food intake (P < 0·01) and an increase in leptin production (P < 0·05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0·05) which could be secondary to the inhibition of the adipogenic transcription factor PPARγ gene expression (P < 0·001), and also to the increase in apoptosis (P < 0·05) found in rats fed with a control diet. TNFα gene expression was significantly increased (P < 0·05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0·01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFα and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

scholarly journals Parameters of Glucose Homeostasis in the Recognition of the Metabolic Syndrome in Young Adults with Prader–Willi Syndrome

2021 ◽  
Vol 10 (23) ◽  
pp. 5635
Author(s):  
Graziano Grugni ◽  
Antonio Fanolla ◽  
Fiorenzo Lupi ◽  
Silvia Longhi ◽  
Antonella Saezza ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Glucose Homeostasis ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Prader Willi Syndrome ◽  
Insulinogenic Index ◽  
Glucose Levels ◽  
The Metabolic Syndrome ◽  
Diagnostic Threshold ◽  
Age Related

To verify the accuracy of different indices of glucose homeostasis in recognizing the metabolic syndrome in a group of adult patients with Prader–Willi syndrome (PWS), 102 PWS patients (53 females/49 males), age ±SD 26.9 ± 7.6 yrs, Body Mass Index (BMI) 35.7 ± 10.7, were studied. The following indices were assessed in each subject during an oral glucose tolerance test (OGTT): 1 h (>155 mg/dL) and 2 h (140–199 mg/dL) glucose levels, the oral disposition index (ODI), the insulinogenic index (IGI), the insulin resistance (HOMA-IR) were evaluated at baseline, 1 h and 2 h. Although minor differences among indices were found, according to the ROC analysis, no index performed better in recognizing MetS. Furthermore, the diagnostic threshold levels changed over the years and therefore the age-related thresholds were calculated. The easily calculated HOMA-IR at baseline may be used to accurately diagnose MetS, thus avoiding more complicated procedures.

scholarly journals Pyroglutamyl leucine, a peptide in fermented foods, attenuates dysbiosis by increasing host antimicrobial peptide

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Saki Shirako ◽  
Yumi Kojima ◽  
Naohiro Tomari ◽  
Yasushi Nakamura ◽  
Yasuki Matsumura ◽  
...  
Keyword(s):  
Body Weight ◽  
Oral Administration ◽  
Antimicrobial Peptide ◽  
High Fat Diet ◽  
Control Diet ◽  
Experimental Colitis ◽  
Fermented Foods ◽  
Food Protein ◽  
High Fat ◽  
Tryptic Fragment

Abstract PyroGlu-Leu is present in certain food protein hydrolysates and traditional Japanese fermented foods. Our previous study demonstrated that the oral administration of pyroGlu-Leu (0.1 mg/kg body weight) attenuates dysbiosis in mice with experimental colitis. The objective of this study was to elucidate why such a low dose of pyroGlu-Leu attenuates dysbiosis in different animal models. High fat diet extensively increased the ratio of Firmicutes/Bacteroidetes in feces of rats compared to control diet. Oral administration of pyroGlu-Leu (1 mg/kg body weight) significantly attenuated high fat diet-induced dysbiosis. By focusing on the production of intestinal antimicrobial peptides, we found that pyroGlu-Leu significantly increased the level of 4962 Da peptides, which identified as the propeptide of rattusin or defensin alpha 9, in ileum. We also observed increased tryptic fragment peptides from rattusin in the lumen. Here, we report that orally administered pyroGlu-Leu attenuates dysbiosis by increasing in the host antimicrobial peptide, rattusin.

scholarly journals Maternal Choline Supplementation Supports Resistance to Effects of Prolonged Western Diet Feeding in Mice Offspring

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1022-1022
Author(s):  
Hunter Korsmo ◽  
Moshe Dembitzer ◽  
Sarah Khaldi ◽  
Shameera Sheeraz ◽  
Juliet Kosichenko ◽  
...  
Keyword(s):  
Maternal Obesity ◽  
De Novo ◽  
Control Diet ◽  
Caloric Intake ◽  
Metabolic Stress ◽  
Acid Synthesis ◽  
Female Offspring ◽  
Western Diet ◽  
High Fat ◽  
Glucose Levels

Abstract Objectives This study investigated whether maternal choline supplementation (MCS) could reduce the chronic metabolic stress that is induced by prenatal maternal obesity and postnatal Western Diet (WD) feeding. Methods C57BL/6 dams were either fed a normal fat (NF, 10 kcal %fat) control diet or a high fat (HF, 45 kcal % fat) diet prior to, during pregnancy and during lactation. These dams received either 25 mM choline or plain drinking water. After weaning, offspring were fed the WD diet (45 kcal %fat, 34 kcal %fructose, and 0.25% cholesterol) for 16 weeks before glucose tolerance testing and dissection. Results After 16 weeks of WD feeding, offspring from normal-fat, choline supplemented fed (MCS-NF) dams are protected from weight gain compared to offspring from dams fed a high-fat diet with or without choline supplementation (MCS-HF or MCO-HF)(P &lt; 0.043). Male offspring from MCS-NF fed dams have reduced caloric intake (P &lt; 0.019) and reduced gene expression of Acc1 which mediates liver de novo fatty acid synthesis (P = 0.005) compared to the non-supplemented normal-fat dams (MCO-NF) after 16 weeks of WD feeding. Female offspring from MCS-HF fed dams have lower fasting glucose levels compared to MCO-HF fed dams after 16 weeks of WD feeding (P = 0.034). Conclusions MCS mitigates some pathological hallmarks that are induced by prolonged WD feeding in offspring. Funding Sources NIGMS.

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