Energy expenditure in obesity-prone and obesity-resistant rats before and after the introduction of a high-fat diet

While most rats gain weight when placed on a high-fat diet (HFD), some strains resist HFD-induced weight gain. To maintain weight, obesity-resistant (OR) rats must either eat less than obesity-prone (OP) rats or increase total energy expenditure (TEE). To determine if changes in TEE predispose to or protect from weight gain, energy expenditure, energy intake, and weight gain were measured in male and female OP and OR rats consuming a low-fat diet (LFD) and for 5 days after switching to a HFD. After 5 days on a HFD, OP rats gained significantly more weight (male: 42.8 ± 6.9 g, female: 25.5 ± 3.0 g) than their OR counterparts (male: 24.0 ± 7.5 g, female: 13.7 ± 1.4 g). Both male and female rats significantly increased their energy intake when transitioned to the HFD, and TEE increased modestly in all groups. Compared with female OP rats, female OR rats had a significantly greater increase in TEE on the HFD. This was due to an increase in both resting and nonresting energy expenditure. In contrast, the effect of the HFD in males was minor. TEE was also measured in female rats consuming a HFD, pair fed to LFD calories. The increase in TEE of pair-fed female OR rats was substantially less than what was seen in the HFD ad libitum condition. Physical activity was also measured in female rats. There was no evidence that increases in physical activity were the cause of the increased TEE seen in female OR rats consuming a HFD. These results suggest that resistance to HFD-induced weight gain in female OR rats may be due in part to an increase in TEE and a greater reliance on lipid as an energy source. Changes in TEE appear to be triggered by overconsumption of the HFD and not simply the diet composition.

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Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Cellular Physiology and Biochemistry ◽

10.1159/000320552 ◽

2010 ◽

Vol 26 (3) ◽

pp. 291-302 ◽

Cited By ~ 47

Author(s):

Antònia Nadal-Casellas ◽

Emilia Amengual-Cladera ◽

Ana María Proenza ◽

Isabel Lladó ◽

Magdalena Gianotti

Keyword(s):

Mitochondrial Biogenesis ◽

High Fat Diet ◽

Female Rats ◽

High Fat ◽

Male And Female ◽

Male And Female Rats

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Kappa-Carrageenan Inhibited the High-Fat-Diet-Induced Obesity Through Up-Regulating the Hepatic Sirt1 Gene Expression

Current Developments in Nutrition ◽

10.1093/cdn/nzab041_018 ◽

2021 ◽

Vol 5 (Supplement_2) ◽

pp. 503-503

Author(s):

Zhiji Huang ◽

Yafang Ma ◽

Chunbao Li

Keyword(s):

Gene Expression ◽

Weight Gain ◽

Energy Expenditure ◽

Energy Intake ◽

High Fat Diet ◽

The Body ◽

High Fat ◽

Diet Induced Obesity ◽

Sirt1 Gene ◽

Kappa Carrageenan

Abstract Objectives Kappa-Carrageenan(CGN) is a widely used food additive in the meat industry and a highly viscous soluble dietary fiber which can hardly be fermented. It has been shown to be able to regulate the energy metabolism and inhibit diet-induced obesity. However, the mechanism is not well understood. The purpose of this study is to investigate the mechanisms of κ-carrageenan to inhibit the body weight gain. Methods A high-fat diet incorporated with lard, pork protein and CGN (2% or 4%, w/w) was given to C57BL/6J mice for 90 days. The energy intake and weight changes were measured every three days. After the dietary intervention, mice were sacrificed, liver and epididymal adipose tissues were taken for real-time polymerase chain reaction (RT-qPCR) analysis. Results The CGN in the high-fat diet restricted weight gain by decreasing liver and adipose mass without inhibiting energy intake. The genes involving energy expenditure such as Acox1, Acadl, CPT-1A and Sirt1 were upregulated in the mice fed with carrageenan. However, the genes responsible for lipid synthesis were not significantly different compared to the diet-induced obese model. Conclusions The anti-obesity effect of the CGN in high-fat diet could be highly related to the enhancement of energy expenditure through up-regulating the downstream genes which promote β-oxidation by increasing the Sirt1 gene expression in liver. Funding Sources Ministry of Science and Technology of the People's Republic of China (10000 Talent Project)

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The Effects of Eating a High Fat Diet on Sensitivity of Male and Female Rats to Methamphetamine and Dopamine D1 Receptor Agonist SKF 82958

Journal of Pharmacology and Experimental Therapeutics ◽

10.1124/jpet.119.263293 ◽

2020 ◽

Vol 374 (1) ◽

pp. 6-15

Author(s):

Jeremiah Ramos ◽

Ethan J. Hardin ◽

Alice H. Grant ◽

Grace Flores-Robles ◽

Adrian T. Gonzalez ◽

...

Keyword(s):

High Fat Diet ◽

Receptor Agonist ◽

Dopamine D1 Receptor ◽

D1 Receptor ◽

Female Rats ◽

High Fat ◽

Male And Female ◽

Male And Female Rats ◽

Skf 82958

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Effect of High-fat Diet on Tracheal Responsiveness to Methacholine and Insulin Resistance Index in Ovalbumin-sensitized Male and Female Rats

Iranian Journal of Allergy Asthma and Immunology ◽

10.18502/ijaai.v18i1.630 ◽

2019 ◽

Author(s):

Hassan Ghobadi ◽

Mohammad Reza Alipour ◽

Rana Keyhanmanesh ◽

Mohammad Hossein Boskabady ◽

Mohammad Reza Aslani

Keyword(s):

Insulin Resistance ◽

High Fat Diet ◽

Close Association ◽

Serum Insulin ◽

Resistance Index ◽

Normal Diet ◽

Female Rats ◽

High Fat ◽

Male And Female ◽

Male And Female Rats

Epidemiological and clinical studies have demonstrated a close association between obesity and asthma. The current study investigated the effect of high-fat diet on tracheal responsiveness to methacholine and insulin resistance in ovalbumin (OVA) sensitized male and female rats. The rats were divided into eight groups (n=6 per group): female with the normal diet (F+ND), male with the normal diet (M+ND), female OVA-sensitized with the normal diet (F+SND), male OVA-sensitized with the normal diet (M+SND), female with high-fat diet (F+HFD), male with high-fat diet (M+HFD), female OVA-sensitized with high-fat diet (F+SHFD), and male OVA-sensitized with high-fat diet (M+SHFD). All rats were fed for 8 weeks with high-fat diet or standard pelts, and for another 4 weeks, they were sensitized with OVA or saline. At the end of the study, the tracheal responsiveness to methacholine, serum insulin, and blood glucose levels was measured. Also, insulin resistance indexes were determined. OVA-sensitization and diet-induced obesity caused the curve of methacholine concentration response to shifting to the left. In addition, results indicated that the EC50 (the effective concentration of methacholine generating 50% of peak response) in F+SHFD rats was statistically lower than M+SHFD group (p<0.05). Moreover, insulin resistance was higher in the F+SHFD than the M+SHFD group (p<0.001). These results suggest that insulin resistance and metabolic syndrome may be involved in the pathogenesis of obesity associated with OVA-sensitized rats condition, especially in female animals.

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Effects of Diet-Induced Obesity on Hypothalamic Kisspeptin-Neurokinin-Dynorphin (KNDy) Neurons and Luteinizing Hormone Secretion in Sex Hormone-Primed Male and Female Rats

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1094 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A537-A537

Author(s):

Shiori Minabe ◽

Kinuyo Iwata ◽

Hitoshi Ozawa

Keyword(s):

Gene Expression ◽

Luteinizing Hormone ◽

High Fat Diet ◽

Female Rats ◽

Male Rats ◽

High Fat ◽

Neurokinin B ◽

Male And Female ◽

Male And Female Rats ◽

Kndy Neurons

Abstract Metabolic stress resulting from a nutrient excess causes infertility in both sexes. Kisspeptin-neurokinin B-dynorphin (KNDy) neurons in the arcuate nucleus (ARC) have been suggested to be key players in reproduction via direct stimulation of gonadotropin-releasing hormone (GnRH) and subsequent gonadotropin release in mammalian species. In this study, we investigated the sex differences in the effects of a high-fat diet (HFD) on KNDy-associated gene expression in the ARC to determine the pathogenic mechanism underlying obesity-induced infertility. Wistar-Imamichi strain male and female rats (7 weeks of age) were fed either a standard diet (10% calories from fat) or high-fat diet (45% calories from fat) for 4 months. In male rats, the HFD caused a significant suppression of Kiss1(encoding kisspeptin), Tac3(encoding neurokinin B), and Pdyn(encoding dynorphin A) gene expression in the ARC, resulting in a decrease in plasma luteinizing hormone (LH) levels. In female rats, 58% of the HFD-fed female rats exhibited irregular estrous cycles, while the other rats showed regular cycles. LH pulses were found, and the numbers of ARC Kiss1-,Tac3-, and Pdyn-expressing cells were high in control animals and almost allHFD-fed female rats, but two out of 10 rats showed profound HFD-induced suppression of LH pulse frequency and reduction in these cells. No statistical differences in LH secretion or ARC KNDy gene expression were observed between HFD-fed and control female rats. Additionally, the number of Gnrh1-expressing cells in the preoptic area was comparable between the groups in both sexes. Our findings revealed that HFD-fed male rats showed KNDy-dependent infertility, while irregular menstruation was mainly induced by KNDy-independent pathways during the incipient stage of obese infertility in female rats. Taken together, hypothalamic kisspeptin neurons in male rats may be susceptible to HFD-induced obesity compared with those in female rats.

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Divergent Energy Expenditure Impacts Mouse Metabolic Adaptation to Acute High-Fat/High-Sucrose Diet Producing Sexually Dimorphic Weight Gain Patterns

10.1101/840702 ◽

2019 ◽

Author(s):

E. Matthew Morris ◽

Roberto D. Noland ◽

Julie A. Allen ◽

Colin S. McCoin ◽

Qing Xia ◽

...

Keyword(s):

Body Composition ◽

Weight Gain ◽

Energy Balance ◽

Energy Expenditure ◽

Energy Intake ◽

Fat Mass ◽

High Fat ◽

Male And Female ◽

Female Mice ◽

High Sucrose

ABSTRACTObjectiveLong-term weight gain can result from cumulative small weight increases due to short-term excess caloric intake during weekends and holidays. Increased physical activity may mediate weight gain through increases in energy expenditure (EE) and reductions in energy balance. Current methods for modulating mouse EE (e.g. – exercise, chemical uncouplers, etc.) have confounding effects. However, it is known that mouse EE linearly increases as housing temperature decreases below the thermoneutral zone.MethodsTo determine how robust differences in baseline EE impact 7-day changes in weight and body composition on low-fat and high-fat, high-sucrose (HFHS) diets, we performed indirect calorimetry measurements in male and female mice housed at divergent temperatures (20°C vs. 30°C).ResultsAs expected, mice housed at 30°C have ∼40% lower total EE and energy intake compared to 20°C mice regardless of diet or sex. Energy balance was increased with HFHS in all groups, with ∼30% greater increases observed in 30°C versus 20°C mice. HFHS increased weight gain regardless of temperature or sex. Interestingly, no HFHS-induced weight gain differences were observed between females at different temperatures. In contrast, 30°C male mice on HFHS gained ∼50% more weight than 20°C males, and ∼80% more weight compared to 30°C females. HFHS increased fat mass across all groups but 2-fold higher gains occurred in 30°C mice compared to 20°C mice. Females gained ∼35% less fat mass than males at both temperatures.ConclusionsTogether, these data reveal an interaction between divergent ambient temperature-induced EE and sex that impacted diet-induced patterns of short-term weight gain and body composition.HighlightsUtilized ambient temperature differences as an experimental tool to study the impact of divergent baseline energy expenditure on metabolic adaptation to high-fat, high-sucrose diet.Baseline energy expenditure and sex interact to impact diet-induced changes in body composition and weight gain.The energy expenditure and sex interaction is a result of an inverse relationship between fat mass gain and weight-adjusted total energy expenditure, as well as, diet-induced non-shivering thermogenesis.These data support that the hypothesis that higher energy expenditure amplifies the coupling of energy intake to energy expenditure during energy dense feeding, resulting in reduced positive energy balance and reduced gains in weight and adiposity.First evidence that energy expenditure level plays a role in the composition of weight gained by female mice during acute HFHS feeding.This study further highlights issues with obesity/energy metabolism research performed in mice at sub-thermoneutral housing temperatures, particularly with sex comparisons.GRAPHIC ABSTRACTLegend: Male and female mice housed at 30°C had lower energy expenditure (EE) & energy intake (EI), while having greater energy balance (EB), during 7-day high-fat/high-sucrose (HFHS) feeding compared to male and female mice, respectively, housed at 20°C. However, female mice had lower EB compared to males at both housing temperature. Female mice housed at 30°C gained less weight than 30°C males but gained the same relative amount of fat mass during acute HFHS feeding. Interestingly, 20°C females gained the same amount of weight as 20°C males but gained primarily fat-free mass, while the males gained the same proportion of fat as 30°C males and females.

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