scholarly journals Voluntary exercise improves hypothalamic and metabolic function in obese mice

2016 ◽  
Vol 229 (2) ◽  
pp. 109-122 ◽  
Author(s):  
Brenton T Laing ◽  
Khoa Do ◽  
Tomoko Matsubara ◽  
David W Wert ◽  
Michael J Avery ◽  
...  
Keyword(s):  
Body Weight ◽  
Exercise Training ◽  
Body Weight Gain ◽  
Critical Role ◽  
Training Group ◽  
Voluntary Exercise ◽  
Whole Body ◽  
Chow Diet ◽  
Metabolic Function ◽  
Leptin Sensitivity

Exercise plays a critical role in regulating glucose homeostasis and body weight. However, the mechanism of exercise on metabolic functions associated with the CNS has not been fully understood. C57BL6 male mice (n=45) were divided into three groups: normal chow diet, high-fat diet (HFD) treatment, and HFD along with voluntary running wheel exercise training for 12 weeks. Metabolic function was examined by the Comprehensive Lab Animal Monitoring System and magnetic resonance imaging; phenotypic analysis included measurements of body weight, food intake, glucose and insulin tolerance tests, as well as insulin and leptin sensitivity studies. By immunohistochemistry, the amount changes in the phosphorylation of signal transducer and activator of transcription 3, neuronal proliferative maker Ki67, apoptosis positive cells as well as pro-opiomelanocortin (POMC)-expressing neurons in the arcuate area of the hypothalamus was identified. We found that 12 weeks of voluntary exercise training partially reduced body weight gain and adiposity induced by an HFD. Insulin and leptin sensitivity were enhanced in the exercise training group verses the HFD group. Furthermore, the HFD-impaired POMC-expressing neuron is remarkably restored in the exercise training group. The restoration of POMC neuron number may be due to neuroprotective effects of exercise on POMC neurons, as evidenced by altered proliferation and apoptosis. In conclusion, our data suggest that voluntary exercise training improves metabolic symptoms induced by HFD, in part through protected POMC-expressing neuron from HFD and enhanced leptin signaling in the hypothalamus that regulates whole-body energy homeostasis.

scholarly journals Early postweaning exercise improves central leptin sensitivity in offspring of rat dams fed high-fat diet during pregnancy and lactation

2013 ◽  
Vol 305 (9) ◽  
pp. R1076-R1084 ◽  
Author(s):  
Bo Sun ◽  
Nu-Chu Liang ◽  
Erin R. Ewald ◽  
Ryan H. Purcell ◽  
Gretha J. Boersma ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Weight Gain ◽  
Metabolic Phenotype ◽  
Chow Diet ◽  
Free Access ◽  
Sprague Dawley ◽  
High Fat ◽  
Leptin Sensitivity ◽  
Pregnancy And Lactation

Maternal high-fat (HF) diet has long-term consequences on the metabolic phenotype of the offspring. Here, we determined the effects of postweaning exercise in offspring of rat dams fed HF diet during gestation and lactation. Pregnant Sprague-Dawley rats were maintained on chow or HF diet throughout gestation and lactation. All pups were weaned onto chow diet on postnatal day (PND) 21. At 4 wk of age, male pups were given free access to running wheels (RW) or remained sedentary (SED) for 3 wk, after which all rats remained sedentary, resulting in four groups: CHOW-SED, CHOW-RW, HF-SED, and HF-RW. Male HF offspring gained more body weight by PND7 compared with CHOW pups and maintained this weight difference through the entire experiment. Three weeks of postweaning exercise did not affect body weight gain in either CHOW or HF offspring, but reduced adiposity in HF offspring. Plasma leptin was decreased at the end of the 3-wk running period in HF-RW rats but was not different from HF-SED 9 wk after the exercise period ended. At 14 wk of age, intracerebroventricular injection of leptin suppressed food intake in CHOW-SED, CHOW-RW, and HF-RW, while it did not affect food intake in HF-SED group. At death, HF-RW rats also had higher leptin-induced phospho-STAT3 level in the arcuate nucleus than HF-SED rats. Both maternal HF diet and postweaning exercise had effects on hypothalamic neuropeptide and receptor mRNA expression in adult offspring. Our data suggest that postweaning exercise improves central leptin sensitivity and signaling in this model.

scholarly journals Interleukin-6 mediated exercise-induced alleviation of adiposity and hepatic steatosis in mice

2021 ◽  
Vol 9 (1) ◽  
pp. e001431
Author(s):  
Long Li ◽  
Caoxin Huang ◽  
Hongyan Yin ◽  
Xiaofang Zhang ◽  
Dongmei Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Hepatic Steatosis ◽  
Interleukin 6 ◽  
Body Weight Gain ◽  
Treadmill Running ◽  
Alcoholic Fatty Liver ◽  
Fat Accumulation ◽  
Ppar Γ

IntroductionExercise training has been shown to be the most effective strategy to combat obesity and non-alcoholic fatty liver disease. However, exercise promotes loss of adipose tissue mass and improves obesity-related hepatic steatosis through mechanisms that remain obscure.Research design and methodsTo study the role of interleukin-6 (IL-6) in high-fat diet (HFD)-induced adiposity and hepatic steatosis during treadmill running, IL-6 knockout (IL-6 KO) mice and wild-type (WT) mice were randomly divided into lean, obese (fed a HFD) and trained obese groups (fed a HFD and exercise trained).ResultsAfter 20 weeks of HFD feeding and 8 weeks of treadmill running, we found that exercise obviously reduced HFD-induced body weight gain, inhibited visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) expansion and almost completely reversed obesity-related intrahepatic fat accumulation in WT mice. However, IL-6 knockout (IL-6 KO) mice are refractory to the benefits of treadmill training on body weight, VAT and SAT mass elevation, and hepatic steatosis. Moreover, a panel of lipolytic-related and thermogenic-related genes, including ATGL, HSL and PGC-1α, was upregulated in the VAT and SAT of WT mice that received exercise training compared with untrained mice, which was not observed in IL-6 KO mice. In addition, exercise training resulted in a significant inhibition of hepatic peroxisome proliferator-activated receptor gamma (PPAR-γ) expression in WT mice, and these effects were not noted in IL-6 KO mice.ConclusionThese results revealed that IL-6 is involved in the prevention of obesity and hepatic fat accumulation during exercise training. The mechanisms underlying these antiobesity effects may be associated with enhanced lipolysis and thermogenesis in white adipose tissue. The improvement in hepatic steatosis by exercise training may benefit from the marked inhibition of PPAR-γ expression by IL-6.

scholarly journals Chronic photoperiodic manipulation induced chronodisruption upregulates HSP60 during early pro-atherogenic remodeling in thoracic aorta of C57BL/6J mice

2021 ◽  
Vol 82 (1) ◽  
Author(s):  
Kavita Shirsath ◽  
Apeksha Joshi ◽  
Aliasgar Vohra ◽  
Ranjitsinh Devkar
Keyword(s):  
Body Weight ◽  
Thoracic Aorta ◽  
Serum Lipid ◽  
Body Weight Gain ◽  
Hdl Cholesterol ◽  
Circadian Disruption ◽  
Control Group ◽  
Chow Diet ◽  
Heat Shock Protein 60 ◽  
Lipid Parameters

Abstract Background Circadian disruption is often associated with aggravation of atherosclerosis; however, the pathophysiological mechanisms underlying atherogenic initiation in normolipidemic diet remains unclear. Most of the studies done for understanding circadian disruption induced atherosclerosis have been carried out in murine model of hyperlipidemia induced atherosclerosis. The present study investigates pro-atherogenic events in response to chronic photoperiodic manipulation induced chronodisruption (PMCD) in C57BL/6J mice fed with laboratory chow diet. Results The results were compared with atherogenic initiation induced by high fat high fructose (HFHF) diet. The combined effects of HFHF and PMCD on atherogenic initiation were also investigated for possible synergy of both variants. The HFHF and HFHF+PMCD groups recorded increments in body weight gains and serum lipid parameters (TC, TG, LDL-cholesterol, VLDL) and a decrement in HDL-cholesterol as compared to the control group. However, PMCD group recorded body weight gain similar to that of the control group, but the serum lipid parameters (TG and VLDL) were significantly elevated and the HDL levels were lowered. However, prominent hypertrophic remodeling, higher collagen deposition, and elastin derangement, along with endothelial dysfunction, its activation, and macrophage infiltration, were observed in thoracic aorta of all the three experimental groups. But the mRNA and immunoblots of heat shock protein 60 (HSP60) in thoracic aorta was found to be maximum in PMCD followed by HFHF and HFHF+PMCD groups. Conclusion Laboratory chow feeding coupled with photoperiodic manipulation mediated chronodisruption overexpress HSP60 that in turn plays a central role in PMCD mediated pro-atherogenic remodeling in thoracic aorta of C57BL/6J mice.

Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle

2021 ◽  
Author(s):  
Tai-Yu Huang ◽  
Melissa A. Linden ◽  
Scott E. Fuller ◽  
Felicia R Goldsmith ◽  
Jacob Simon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Exercise Training ◽  
Fat Mass ◽  
Mitochondrial Fission ◽  
Critical Role ◽  
Oxidative Capacity ◽  
Low Fat Diet ◽  
Ketogenic Diets ◽  
Diet And Exercise

Ketogenic diets (KD) are reported to improve body weight, fat mass, and exercise performance in humans. Unfortunately, most rodent studies have used a low-protein KD, which does not recapitulate diets used by humans. Since skeletal muscle plays a critical role in responding to macronutrient perturbations induced by diet and exercise, the purpose of this study was to test if a normal-protein KD (NPKD) impacts shifts in skeletal muscle substrate oxidative capacity in response to exercise training (ExTr). A high fat, carbohydrate-deficient NPKD (16.1% protein, 83.9% fat, 0% carbohydrate) was given to C57BL/6J male mice for 6 weeks, while controls received a low fat diet with similar protein (15.9% protein, 11.9% fat, 72.2% carbohydrate). On week four of the diet, mice began treadmill training 5 days/week, 60 min/day for 3 weeks. NPKD-fed mice increased body weight and fat mass, while ExTr negated a continued rise in adiposity. ExTr increased intramuscular glycogen, while the NPKD increased intramuscular triglycerides. Neither the NPKD nor ExTr alone altered mitochondrial content; however, in combination, the NPKD-ExTr group showed increases in PGC-1α, as well as markers of mitochondrial fission and fusion. Pyruvate oxidative capacity was unchanged by either intervention, while ExTr increased leucine oxidation in NPKD-fed mice. Lipid metabolism pathways had the most notable changes as the NPKD and ExTr interventions both enhanced mitochondrial and peroxisomal lipid oxidation and many adaptations were additive or synergistic. Overall these results suggest a combination of a NPKD and ExTr induces additive and/or synergistic adaptations in skeletal muscle oxidative capacity.

Effect of exercise training on energy balance of orchidectomized rats

1989 ◽  
Vol 257 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
S. Rivest ◽  
J. Landry ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
Cytochrome C ◽  
Exercise Training ◽  
Protein Content ◽  
Cytochrome C Oxidase ◽  
Oxidase Activity ◽  
Body Weight Gain ◽  
Energy Gain

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and testosterone on energy balance. Male rats were divided into sedentary and exercise-trained groups. Each group formed was further divided into a sham-operated group, an orchidectomized group, or an orchidectomized group treated with testosterone. Rats were exercised on a motor-driven treadmill for 1 h/day over 28 consecutive days, after which rats were killed. Energy balance measurements, body composition analyses, and serum testosterone assay were then performed. The weight, protein content, and cytochrome-c oxidase activity of interscapular brown adipose tissue (IBAT) were also measured. Results indicate that total food intake, final body weight, and body weight gain were generally lower in exercise-trained rats than in sedentary animals. In orchidectomized rats treated with testosterone, gains of both fat and protein were lower in exercise-trained than in sedentary animals. There was no difference in metabolizable energy intake and body energy gain between trained and sedentary rats that underwent orchidectomy without replacement therapy. In orchidectomized groups of rats, energy gain was lower in trained rats that were treated with testosterone than in those that did not receive any treatment. Furthermore, in trained orchidectomized rats treated with testosterone, both energetic efficiency and energy density of body weight gain were lower than those of trained orchidectomized rats that were not treated. Finally, a significant reduction in IBAT weight was observed in exercise-trained animals, whereas neither exercise nor the various hormonal manipulations affected IBAT protein content and cytochrome-c oxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The accretion of copper and of zinc by the foetuses of prolific ewes

1978 ◽  
Vol 40 (2) ◽  
pp. 377-386 ◽  
Author(s):  
R. B. Williams ◽  
I. McDonald ◽  
I. Bremner
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Live Weight ◽  
Whole Body ◽  
Live Weight Gain ◽  
Unit Body Weight ◽  
Growth Equations ◽  
Total Body ◽  
Cu And Zn

1. The amounts of copper and zinc in the foetuses of ewes carrying from one to four lambs were measured at different stages of gestation and estimates were made of the amounts of these metals in their livers.2. The accretion of Cu and Zn could be described by growth equations of the Gompertz form, from which could be derived estimates of the instantaneous and fractional rates of deposition of these metals in the foetal body.3. Between the 80th and 144th day of gestation the instantaneous rates of deposition of the metals increased exponentially, and at the end of pregnancy were calculated to be 0.24 and 2.0 mg Cu and Zn/d respectively in the triplet lamb foetus. The corresponding total accretions were estimated to be 10 and 69 mg respectively.4. The fractional rates of live-weight gain and of deposition of Cu were similar and decreased at similar rates; that of Zn deposition decreased much more slowly.5. The proportion of whole-body Cu estimated to be in the liver was always greater than 50 %. The amount of Zn in the liver remained constant and contributed 72 % of the total body Zn at 80 d but only 8 % at 144d.6. The relative amounts of Cu and of Zn accrued per unit body-weight gain were not constant during the development of the foetus. As foetal numbers increased the amounts of each metal deposited in the foetus decreased more rapidly than did foetal weight.7. The results are discussed in relation to the demands for Cu and Zn during pregnancy in sheep.

scholarly journals Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

2007 ◽  
Vol 293 (3) ◽  
pp. R1056-R1062 ◽  
Author(s):  
Jacqueline Férézou-Viala ◽  
Anne-France Roy ◽  
Colette Sérougne ◽  
Daniel Gripois ◽  
Michel Parquet ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Weight Gain ◽  
Maternal Diet ◽  
The Body ◽  
Female Rats ◽  
Leptin Resistance ◽  
High Fat ◽  
Leptin Sensitivity ◽  
The Impact

Epidemiological and animal studies suggest that the alteration of hormonal and metabolic environment during fetal and neonatal development can contribute to development of metabolic syndrome in adulthood. In this paper, we investigated the impact of maternal high-fat (HF) diet on hypothalamic leptin sensitivity and body weight gain of offspring. Adult Wistar female rats received a HF or a control normal-fat (C) diet for 6 wk before gestation until the end of the suckling period. After weaning, pups received either C or HF diet during 6 wk. Body weight gain and metabolic and endocrine parameters were measured in the eight groups of rats formed according to a postweaning diet, maternal diet, and gender. To evaluate hypothalamic leptin sensitivity in each group, STAT-3 phosphorylation was measured in response to leptin or saline intraperitoneal bolus. Pups exhibited similar body weights at birth, but at weaning, those born to HF dams weighed significantly less (−12%) than those born to C dams. When given the HF diet, males and females born to HF dams exhibited smaller body weight and feed efficiency than those born to C dams, suggesting increased energy expenditure programmed by the maternal HF diet. Thus, maternal HF feeding could be protective against adverse effects of the HF diet as observed in male offspring of control dams: overweight (+17%) with hyperleptinemia and hyperinsulinemia. Furthermore, offspring of HF dams fed either C or HF diet exhibited an alteration in hypothalamic leptin-dependent STAT-3 phosphorylation. We conclude that maternal high-fat diet programs a hypothalamic leptin resistance in offspring, which, however, fails to increase the body weight gain until adulthood.

Dorsomedial hypothalamic corticotropin-releasing factor mediation of exercise-induced anorexia

2005 ◽  
Vol 288 (6) ◽  
pp. R1800-R1805 ◽  
Author(s):  
Maiko Kawaguchi ◽  
Karen A. Scott ◽  
Timothy H. Moran ◽  
Sheng Bi
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Food Intake ◽  
Mrna Expression ◽  
Critical Role ◽  
Voluntary Exercise ◽  
Running Wheel ◽  
Exercise Induced ◽  
Running Wheels ◽  
Induced Changes

Running wheel access and resulting voluntary exercise alter food intake and reduce body weight. The neural mechanisms underlying these effects are unclear. In this study, we first assessed the effects of 7 days of running wheel access on food intake, body weight, and hypothalamic gene expression. We demonstrate that running wheel access significantly decreases food intake and body weight and results in a significant elevation of CRF mRNA expression in the dorsomedial hypothalamus (DMH) but not the paraventricular nucleus. Seven-day running wheel access also results in elevated arcuate nucleus and DMH neuropeptide Y gene expression. To assess a potential role for elevated DMH CRF activity in the activity-induced changes in food intake and body weight, we compared changes in food intake, body weight, and hypothalamic gene expression in rats receiving intracerebroventricular (ICV) CRF antagonist α-helical CRF or vehicle with or without access to running wheels. During a 4-day period of running wheel access, we found that exercise-induced reductions of food intake and body weight were significantly attenuated by ICV injection of the CRF antagonist. The effect on food intake was specific to a blockade of activity-induced changes in meal size. Central CRF antagonist injection further increased DMH CRF mRNA expression in exercised rats. Together, these data suggest that DMH CRF play a critical role in the anorexia resulting from increased voluntary exercise.

Fish-meal supplementation of grass silage offered to young steers: Effects on growth, body composition and nutrient efficiency

2001 ◽  
Vol 137 (1) ◽  
pp. 85-96 ◽  
Author(s):  
R. SANDERSON ◽  
M. S. DHANOA ◽  
C. THOMAS ◽  
A. B. McALLAN
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Weight Gain ◽  
Fish Meal ◽  
Body Weight Gain ◽  
Live Weight ◽  
Metabolizable Energy ◽  
Energy Utilization ◽  
Whole Body ◽  
Nitrogen Intake

Growth and efficiencies of nitrogen and energy utilization for growth by 72 young British Friesian steers (initial live weight (LW) 110 kg) offered a well preserved, formic acid-treated, perennial ryegrass silage with and without supplements of fish meal were examined. Silage was offered either alone or mixed with 50, 100 or 150 g fish meal/kg silage dry matter (DM) and each diet was offered either ad libitum or intakes were restricted to 16, 19 or 22 g dietary DM/kg LW/day. Treatments were imposed over a period of 132 days. Body component weight gains were determined by comparative slaughter.Increasing the level of either feeding or fish meal increased rates of empty body weight gain linearly (P<0·001) and curvilinearly (P<0·05) respectively. Fish-meal supplementation increased rates of ash and crude protein gain (P<0·001) but, in comparison with the curvilinear response to increasing level of feeding (P<0·001), had small linear effects on fat gain (P>0·01). Consequently, in terms of whole body composition, animals given fish meal were leaner than animals offered silage alone. Fish-meal supplementation had no significant effect on the composition of the carcass but increased the concentration of protein in the liver and gastrointestinal tract.The increase in nitrogen intake associated with feeding fish meal resulted in a reduction in the efficiency of nitrogen utilization as level of fish meal increased. Nitrogen intake required for maintenance was estimated to be 1·054 g/kg LW0·75. In spite of marked differences in the composition of the empty body-weight gain, there was no evidence to support an effect of fish meal on the efficiency of metabolizable energy (ME) utilization for growth (kf) which was estimated to be 0·346 on the basis of data scaled by LW0·75. ME intake required for maintenance (MEm) was estimated to be 0·536 and 0·502 MJ/kg LW0·75 for silage alone and the 150 g fish-meal level respectively.

scholarly journals A combination of exercise and capsinoid supplementation additively suppresses diet-induced obesity by increasing energy expenditure in mice

2015 ◽  
Vol 308 (4) ◽  
pp. E315-E323 ◽  
Author(s):  
Kana Ohyama ◽  
Yoshihito Nogusa ◽  
Katsuya Suzuki ◽  
Kosaku Shinoda ◽  
Shingo Kajimura ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Body Weight Gain ◽  
Whole Body ◽  
Voluntary Running ◽  
Running Wheel Exercise ◽  
Body Energy

Exercise effectively prevents the development of obesity and obesity-related diseases such as type 2 diabetes. Capsinoids (CSNs) are capsaicin analogs found in a nonpungent pepper that increase whole body energy expenditure. Although both exercise and CSNs have antiobesity functions, the effectiveness of exercise with CSN supplementation has not yet been investigated. Here, we examined whether the beneficial effects of exercise could be further enhanced by CSN supplementation in mice. Mice were randomly assigned to four groups: 1) high-fat diet (HFD, Control), 2) HFD containing 0.3% CSNs, 3) HFD with voluntary running wheel exercise (Exercise), and 4) HFD containing 0.3% CSNs with voluntary running wheel exercise (Exercise + CSN). After 8 wk of ingestion, blood and tissues were collected and analyzed. Although CSNs significantly suppressed body weight gain under the HFD, CSN supplementation with exercise additively decreased body weight gain and fat accumulation and increased whole body energy expenditure compared with exercise alone. Exercise together with CSN supplementation robustly improved metabolic profiles, including the plasma cholesterol level. Furthermore, this combination significantly prevented diet-induced liver steatosis and decreased the size of adipocyte cells in white adipose tissue. Exercise and CSNs significantly increased cAMP levels and PKA activity in brown adipose tissue (BAT), indicating an increase of lipolysis. Moreover, they significantly activated both the oxidative phosphorylation gene program and fatty acid oxidation in skeletal muscle. These results indicate that CSNs efficiently promote the antiobesity effect of exercise, in part by increasing energy expenditure via the activation of fat oxidation in skeletal muscle and lipolysis in BAT.

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