scholarly journals Exercise training alters effect of high-fat feeding on the ACTH stress response in pigs

2008 ◽  
Vol 33 (3) ◽  
pp. 461-469 ◽  
Author(s):  
Ryan Jankord ◽  
Venkataseshu K. Ganjam ◽  
James R. Turk ◽  
Marc T. Hamilton ◽  
M. Harold Laughlin

Eating and physical activity behaviors influence neuroendocrine output. The purpose of this study was to test, in an animal model of diet-induced cardiovascular disease, the effects of high-fat feeding and exercise training on hypothalamo–pituitary–adrenocortical (HPA) axis activity. We hypothesized that a high-fat diet would increase circulating free fatty acids (FFAs) and decrease the adrenocorticotropic hormone (ACTH) and cortisol response to an acute stressor. We also hypothesized that exercise training would reverse the high-fat diet-induced changes in FFAs and thereby restore the ACTH and cortisol response. Pigs were placed in 1 of 4 groups (normal diet, sedentary; normal diet, exercise training; high-fat diet, sedentary; high-fat diet, exercise training; n = 8/group). Animals were placed on their respective dietary and activity treatments for 16–20 weeks. After completion of the treatments animals were anesthetized and underwent surgical intubation. Blood samples were collected after surgery and the ACTH and cortisol response to surgery was determined and the circulating concentrations of FFAs, glucose, cholesterol, insulin, and IGF-1 were measured. Consistent with our hypothesis, high-fat feeding increased FFAs by 200% and decreased the ACTH stress response by 40%. In exercise-trained animals, the high-fat diet also increased FFA; however, the increase in FFA in exercise-trained pigs was accompanied by a 60% increase in the ACTH response. The divergent effect of high-fat feeding on ACTH response was not expected, as exercise training alone had no effect on the ACTH response. Results demonstrate a significant interaction between diet and exercise and their effect on the ACTH response. The divergent effects of high-fat diet could not be explained by changes in weight gain, blood glucose, insulin, or IGF-1, as these were altered by high-fat feeding, but unaffected by exercise training. Thus, the increase in FFA with high-fat feeding may explain the blunted ACTH response to an acute stressor in sedentary animals, but cannot explain the exaggerated response in exercise trained animals.

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Yumeng Bai ◽  
Yali Feng ◽  
Bo Jiang ◽  
Yan Yang ◽  
Zuowei Pei ◽  
...  

Hyperlipidemia causes nervous system-related diseases. Exercise training has developed into an established evidence-based treatment strategy that is beneficial for neuronal injury. This study investigated the effect of exercise on hyperlipidemia-induced neuronal injury in apolipoprotein E-deficient (ApoE-/-) mice. Male ApoE-/- mice (age: 8 weeks) were randomly divided into four groups as follows: mice fed a normal diet (ND), normal diet+swimming training (ND+S), high-fat diet (HD), and high-fat diet+swimming (HD+S). Exercise training consisted of swimming for 40 min/day, 5 days/week for 12 weeks. After 12 weeks, we measured serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c). We also evaluated glial fibrillary acidic protein (GFAP) expression levels using immunohistochemistry, real-time PCR, and immunoblotting. In addition, NLR family pyrin domain-containing 3 (NLRP3), interleukin- (IL-) 18, caspase-1, Bax, Bcl-2, and phosphorylated extracellular signal-regulated kinase (p-ERK) expression levels were measured using immunoblotting. Serum levels of TG, TC, and LDL-c were lower in ApoE-/- HD+S mice than in ApoE-/- HD mice. Immunohistochemistry, real-time PCR, and immunoblotting showed increased levels of GFAP in the ApoE-/- HD group. Immunoblotting revealed increased levels of NLRP3, IL-18, caspase-1, Bax, Bcl-2, and p-ERK in the ApoE-/- HD group; however, they were significantly suppressed in the ApoE-/- HD+S group. Therefore, exercise has protective effects against neuronal injury caused by hyperlipidemia.


2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Yi Yan ◽  
Chunyu Liang ◽  
Rui Xu

Objective To observe the effect of high fat diet on the hypothalamic expression of KiSS-1and the G-protein coupled receptor (GPR) 54 mRNA and explore the modulatory role of moderate-intensity exercise in the diet induced obesity male rats. Methods After 8 weeks high fat feeding, 20 obesity 11-weeks SD rats were randomly assigned to high-fat diet sedentary (FS, n=8) and high-fat diet exercise (FE, n=8) groups, 20 normal diet 11-weeks SD rats also were randomly assigned to sedentary (SS, n=8) and exercise (SE, n=8) groups. During the following 8 weeks, obesity rats were continued expose to high-fat-diet. SE and FE groups did the 60%-70%V(•)O2max treadmill training (5 days/week, 1 hour/day). The V(•)O2 max of exercise groups were remeasured every two weeks. The hypothalamic expression of KiSS-1 and GPR54 mRNA were tested in each group. Results After the first 8-weeks high fat feeding, the obesity rats were heavier than normal diet group (491.74±26.19g vs. 410.05±45.77g, p<0.01). After 8-weeks training, the FE group was lighter than FS group (590.23±35.74g vs. 681±52.56, p<0.01). The FS group had higher hypothalamic expression of KiSS-1 mRNA (1.51±0.66 vs 0.75±0.27, p<0.05) and GPR54 mRNA (2.45±0.38 vs 0.61±0.15, p<0.01) than SS group. The FE group had lower hypothalamic expression of KiSS-1 mRNA (0.69±0.13, p>0.05) and GPR54 mRNA (0.58±0.10, p<0.01) than FS group. Conclusions There is stimulating effect of high-fat diet induced obesity on hypothalamic expression of KiSS-1and GPR54 mRNA. 8-weeks 60%-70%V (•) O2max treadmill training could cure this effect.  


2007 ◽  
Vol 293 (3) ◽  
pp. H1553-H1563 ◽  
Author(s):  
Yan Yang ◽  
Allan W. Jones ◽  
Tom R. Thomas ◽  
Leona J. Rubin

Potassium channels in vascular smooth muscle (VSM) control vasodilation and are potential regulatory targets. This study evaluated effects of sex differences, exercise training (EX), and high-fat diet (HF) on K+ currents ( IK) of coronary VSM cells. Yucatan male and female swine were assigned to either sedentary confinement (SED), 16 wk of EX, 20 wk of HF, or 20 wk of HF with 16 wk of EX (HF-EX). VSM cells of normal-diet SED animals exhibited three components of IK: 4-aminopyridine-sensitive IK(KV), TEA-sensitive IK(BK), and 4-aminopyridine + TEA-insensitive IK. Females exhibited significantly higher basal IK than males in the same group. EX increased basal IK in males and females. HF reduced IK in males and females and nullified effects of EX. Endothelin-1 increased IK significantly in males but not in females. In the presence of endothelin-1, 1) IK(KV) was similar in SED males and females and EX increased IK(KV) to a greater extent in males than in females and 2) IK(BK) was greater in SED females than in males and EX increased IK(BK) to a greater extent in males, resulting in IK(BK) similar to EX females. Importantly, HF nullified effects of EX on IK(KV) and IK(BK). These data indicate that basal IK of SED female swine is inherently greater than that shown in SED males and that males require EX to achieve comparable levels of IK. Importantly, HF reduced IK in males and females and nullified effects of EX, suggesting HF abrogates beneficial effects of EX on coronary smooth muscle.


2011 ◽  
Vol 301 (2) ◽  
pp. R320-R326 ◽  
Author(s):  
Lindsay M. Edwards ◽  
Cameron J. Holloway ◽  
Andrew J. Murray ◽  
Nicholas S. Knight ◽  
Emma E. Carter ◽  
...  

We recently showed that a week-long, high-fat diet reduced whole body exercise efficiency in sedentary men by >10% (Edwards LM, Murray AJ, Holloway CJ, Carter EE, Kemp GJ, Codreanu I, Brooker H, Tyler DJ, Robbins PA, Clarke K. FASEB J 25: 1088–1096, 2011). To test if a similar dietary regime would blunt whole body efficiency in endurance-trained men and, as a consequence, hinder aerobic exercise performance, 16 endurance-trained men were given a short-term, high-fat (70% kcal from fat) and a moderate carbohydrate (50% kcal from carbohydrate) diet, in random order. Efficiency was assessed during a standardized exercise task on a cycle ergometer, with aerobic performance assessed during a 1-h time trial and mitochondrial function later measured using 31P-magnetic resonance spectroscopy. The subjects then underwent a 2-wk wash-out period, before the study was repeated with the diets crossed over. Muscle biopsies, for mitochondrial protein analysis, were taken at the start of the study and on the 5th day of each diet. Plasma fatty acids were 60% higher on the high-fat diet compared with moderate carbohydrate diet ( P < 0.05). However, there was no change in whole body efficiency and no change in mitochondrial function. Endurance exercise performance was significantly reduced ( P < 0.01), most probably due to glycogen depletion. Neither diet led to changes in citrate synthase, ATP synthase, or mitochondrial uncoupling protein 3. We conclude that prior exercise training blunts the deleterious effect of short-term, high-fat feeding on whole body efficiency.


2011 ◽  
Vol 110 (6) ◽  
pp. 1607-1614 ◽  
Author(s):  
Mette Skovbro ◽  
Robert Boushel ◽  
Christina Neigaard Hansen ◽  
Jørn Wulff Helge ◽  
Flemming Dela

Twenty one healthy untrained male subjects were randomized to follow a high-fat diet (HFD; 55–60E% fat, 25–30E% carbohydrate, and 15E% protein) or a normal diet (ND; 25–35E% fat, 55–60E% carbohydrate, and 10–15E% protein) for 21/2 wk. Diets were isocaloric and tailored individually to match energy expenditure. At 21/2 wk of diet, one 60-min bout of bicycle exercise (70% of maximal oxygen uptake) was performed. Muscle biopsies were obtained before and after the diet, immediately after exercise, and after 3-h recovery. Insulin sensitivity (hyperinsulinemic-euglycemic clamp) and intramyocellular triacylglycerol content did not change with the intervention in either group. Indexes of mitochondrial density were similar across the groups and intervention. Mitochondrial respiratory rates, measured in permeabilized muscle fibers, showed a 31 ± 11 and 26 ± 9% exercise-induced increase ( P < 0.05) in state 3 (glycolytic substrates) and uncoupled respiration, respectively. However, in HFD this increase was abolished. At recovery, no change from resting respiration was seen in either group. With a lipid substrate (octanoyl-carnitine with or without ADP), similar exercise-induced increases (31–62%) were seen in HFD and ND, but only in HFD was an elevated ( P < 0.05) respiratory rate seen at recovery. With HFD complex I and IV protein expression decreased ( P < 0.05 and P = 0.06, respectively). A fat-rich diet induces marked changes in the mitochondrial electron transport system protein content and in exercise-induced mitochondrial substrate oxidation rates, with the effects being present hours after the exercise. The effect of HFD is present even without effects on insulin sensitivity and intramyocellular lipid accumulation. An isocaloric high-fat diet does not cause insulin resistance.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kathryn M. Spitler ◽  
Shwetha K. Shetty ◽  
Emily M. Cushing ◽  
Kelli L. Sylvers-Davie ◽  
Brandon S. J. Davies

AbstractElevated plasma triglyceride levels are associated with metabolic disease. Angiopoietin-like protein 4 (ANGPTL4) regulates plasma triglyceride levels by inhibiting lipoprotein lipase (LPL). Our aim was to investigate the role of adipocyte-specific deficiency of ANGPTL4 in mice during high fat diet feeding. Adipocyte-specific ANGPTL4 deficient mice were fed a high fat diet (60% kCal from fat) for either 12 weeks or 6 months. We performed plasma metabolic measurements, triglyceride clearance and uptake assays, LPL activity assays, and assessed glucose homeostasis. Mice lacking adipocyte ANGPTL4 recapitulated the triglyceride phenotypes of whole-body ANGPTL4 deficiency, including increased adipose LPL activity, lower plasma triglyceride levels, and increased uptake of triglycerides into adipose tissue. When fed a high fat diet (HFD), these mice continued to display enhanced adipose LPL activity and initially had improved glucose and insulin sensitivity. However, after 6 months on HFD, the improvements in glucose homeostasis were largely lost. Moreover, despite higher adipose LPL activity levels, mice lacking adipocyte ANGPTL4 no longer had increased triglyceride uptake into adipose compared to littermate controls after chronic high-fat feeding. These observations suggest that after chronic high-fat feeding LPL is no longer rate-limiting for triglyceride delivery to adipocytes. We conclude that while adipocyte-derived ANGPTL4 is an important regulator of plasma triglyceride levels and triglyceride partitioning under normal diet conditions, its role is diminished after chronic high-fat feeding.


2021 ◽  
Vol 22 (2) ◽  
pp. 966
Author(s):  
Seita Osawa ◽  
Hisashi Kato ◽  
Yuki Maeda ◽  
Hisashi Takakura ◽  
Junetsu Ogasawara ◽  
...  

Controlling the differentiation potential of adipose-derived stem cells (ADSCs) is attracting attention as a new strategy for the prevention and treatment of obesity. Here, we aimed to observe the effect of exercise training (TR) and high-fat diet (HFD) on the metabolic profiles of ADSCs-derived adipocytes. The rats were divided into four groups: normal diet (ND)-fed control (ND-SED), ND-fed TR (ND-TR), HFD-fed control (HFD-SED), and HFD-fed TR (HFD-TR). After 9 weeks of intervention, ADSCs of epididymal and inguinal adipose tissues were differentiated into adipocytes. In the metabolome analysis of adipocytes after isoproterenol stimulation, 116 metabolites were detected. The principal component analysis demonstrated that ADSCs-derived adipocytes segregated into four clusters in each fat pad. Amino acid accumulation was greater in epididymal ADSCs-derived adipocytes of ND-TR and HFD-TR, but lower in inguinal ADSCs-derived adipocytes of ND-TR, than in the respective controls. HFD accumulated several metabolites including amino acids in inguinal ADSCs-derived adipocytes and more other metabolites in epididymal ones. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that TR mainly affected the pathways related to amino acid metabolism, except in inguinal ADSCs-derived adipocytes of HFD-TR rats. These findings provide a new way to understand the mechanisms underlying possible changes in the differentiation of ADSCs due to TR or HFD.


Author(s):  
Katsuyuki Tokinoya ◽  
Seiko Ono ◽  
Kai Aoki ◽  
Koki Yanazawa ◽  
Yasuhiro Shishikura ◽  
...  

AbstractIntroductionExercise training is beneficial for reducing obesity. In particular, exercise training can lower the catecholamine concentration in circulation. Renalase, whose expression was first confirmed in the kidneys, is a physiologically active substance that decomposes circulating catecholamines; additionally, it has been reported to be present in the skeletal muscles. The aim of this study was to clarify the expression of renalase in the skeletal muscles and kidneys after high-intensity exercise training in obese mice.Material and methodsThe mice were divided into four groups: normal diet and sedentary, normal diet and exercise training, high-fat diet and sedentary, and high-fat diet and exercise training, and the test was performed for 8 weeks.ResultsBody weight and skeletal muscle wet weight were reduced by high-fat diet intake but were rescued by training. Skeletal muscle renalase gene expression was significantly increased by exercise training. However, in the kidneys the gene expression of renalase was significantly increased by high-fat diet intake and exercise training. No significant changes were observed in the gene expression of catecholamine-degrading enzymes, catechol-O-methyltransferase and monoamine oxidase A and B.ConclusionWe demonstrated that exercise training increased the gene expression of renalase in the skeletal muscles and kidneys, thus lowering circulating catecholamine levels. This may lead to amelioration of obesity as catecholamines are lipolytic.


Obesity Facts ◽  
2021 ◽  
pp. 1-14
Author(s):  
Yi-Ju Hsu ◽  
Chien-Chao Chiu ◽  
Mon-Chien Lee ◽  
Wen-Ching Huang

<b><i>Introduction:</i></b> Obesity, which can result from disease, genetics, nutrition, lifestyle, and insufficient physical activity, substantially increases an individual’s risk of complications and comorbidities. Exercise can be an effective strategy for achieving an energy balance and physiological fitness as part of obesity management. Additionally, probiotics, which are isolated from food and the environment, are being rapidly developed and have functional benefits for mitigating various metabolic dysfunctions associated with obesity. The potentially positive physiological and functional effects of exercise, probiotics, and exercise combined with probiotics should be elucidated in a model of diet-induced obesity. <b><i>Methods:</i></b> <i>Bifidobacterium longum</i> subsp. <i>longum</i> OLP-01 (OLP-01) was isolated from an elite Olympic-level athlete who exhibited physiological adaptations to peripheral fatigue caused by exercise training. In this current study, ICR strain mice were fed a high-fat diet (HFD) for 4 weeks to replicate an obesity model. The mice were divided into 5 groups according to the diet administered: control with normal diet, only HFD, HFD + exercise, HFD + OLP, and HFD + exercise + OLP groups. They were administered the probiotic and/or treadmill exercise training for 5 weeks, and their growth curve, physical activity, physiological adaptation, biochemical parameters, body composition, and glucose tolerance were assessed. <b><i>Results:</i></b> Compared with only exercise or only probiotics, a combination of probiotics and exercise significantly improved the weight, glucose tolerance, fat composition, and exercise-related oxidative stress of mice. Regular and programmed exercise with sufficient rest may be crucial to obesity improvement, and a combination of probiotics and exercise may synergistically assist obesity management and health promotion. <b><i>Conclusion:</i></b> OLP-01 probiotics combined with exercise training can be employed as a strategy for treating obesity. However, the exact regulatory mechanisms underlying this effect, possibly involving microbiota and associated metabolites, warrant further investigation.


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