Influence of dietary fat on some metabolic responses of cattle to hyperthermia induced by heat exposure

1. Two breeds of cattle which differ in their plasma concentrations of lipid components (PCLC) and ability to tolerate heat were used to study metabolic responses to hyperthermia. Two maintenance diets, LF (2.5% Fat) and HF (9.2% Fat), which were isonitrogenous and isocaloric were used. 2. The PCLC, the net esterification of cholesterol by the lecithin: cholesterol acyl transferase system and faecal fat excretion were increased by the HF diet which reduced urinary N loss. 3. Hyperthermia disturbed lipid metabolism in all animals and reductions in the concentrations of plasma cholesterol and phospholipid paralleled the increases in the quantities of fat excreted in the faeces. 4. Within breeds the animals on the HF diet maintained a higher PCLC, lower body temperature and conserved more body nitrogen during hyperthermia than animals on the LF diet. 5. The results point to a role for dietary lipid in ameliorating the metabolic disturbances in animals during chronic hyperthermia.     

Soluble Fermentable Dietary Fibre (Pectin) Decreases Caloric Intake,Adiposity and Lipidaemia in High-Fat Diet-Induced Obese Rats

Consumption of a high fat diet promotes obesity and poor metabolic health, both of which may be improved by decreasing caloric intake. Satiety-inducing ingredients such as dietary fibre may be beneficial and this study investigates in diet-induced obese (DIO) rats the effects of high or low fat diet with or without soluble fermentable fibre (pectin). In two independently replicated experiments, young adult male DIO rats that had been reared on high fat diet (HF; 45% energy from fat) were given HF, low fat diet (LF; 10% energy from fat), HF with 10% w/w pectin (HF+P), or LF with 10% w/w pectin (LF+P) ad libitum for 4 weeks (n = 8/group/experiment). Food intake, body weight, body composition (by magnetic resonance imaging), plasma hormones, and plasma and liver lipid concentrations were measured. Caloric intake and body weight gain were greatest in HF, lower in LF and HF+P, and lowest in the LF+P group. Body fat mass increased in HF, was maintained in LF, but decreased significantly in LF+P and HF+P groups. Final plasma leptin, insulin, total cholesterol and triglycerides were lower, and plasma satiety hormone PYY concentrations were higher, in LF+P and HF+P than in LF and HF groups, respectively. Total fat and triglyceride concentrations in liver were greatest in HF, lower in LF and HF+P, and lowest in the LF+P group. Therefore, the inclusion of soluble fibre in a high fat (or low fat) diet promoted increased satiety and decreased caloric intake, weight gain, adiposity, lipidaemia, leptinaemia and insulinaemia. These data support the potential of fermentable dietary fibre for weight loss and improving metabolic health in obesity.     

Subcutaneous lipectomy causes a metabolic syndrome in hamsters

The insulin resistance syndrome X is related to excess intra-abdominal adipose tissue. With lipectomy of >50% of subcutaneous adipose tissue (SQAT) in nonhibernating, adult female Syrian hamsters on high-fat (HF; 50 calorie%) diet and measurements of oral glucose tolerance, oral [(14)C]oleic acid disposal, serum triglycerides, serum leptin, liver fat, perirenal (PR) adipose tissue cellularity, and body composition, we studied the role of SQAT. Sham-operated (S) animals on HF or low-fat (LF; 12.5 calorie%) diets served as controls. After 3 mo there was no visible regrowth of SQAT but HF diet led to similar levels of body weight and body fat in lipectomized and sham-operated animals. Lipectomized (L) animals had more intra-abdominal fat as a percentage of total body fat, higher insulinemic index, a strong trend toward increased liver fat content, and markedly elevated serum triglycerides compared with S-HF and S-LF. Liver and PR adipose tissue uptake of fatty acid were similar in L-HF and S-HF but reduced vs. S-LF, and were inversely correlated with liver fat content and insulin sums during the oral glucose tolerance test. In summary, lipectomy of SQAT led to compensatory fat accumulation implying regulation of total body fat mass. In conjunction with HF diet these lipectomized hamsters developed a metabolic syndrome with significant hypertriglyceridemia, relative increase in intra-abdominal fat, and insulin resistance. We propose that SQAT, via disposal and storage of excess ingested energy, acts as a metabolic sink and protects against the metabolic syndrome of obesity.     

A 12-week aerobic exercise intervention results in improved metabolic function and lower adipose tissue and ectopic fat in high-fat diet fed rats

Investigations of long-term exercise interventions in humans to reverse obesity is expensive and is hampered by poor compliance and confounders. In the present study, we investigated intrahepatic and muscle fat, visceral and subcutaneous fat pads, plasma metabolic profile and skeletal muscle inflammatory markers in response to 12-week aerobic exercise in an obese rodent model. Six-week-old male Wistar rats (n=20) were randomized to chow-fed control (Control, n=5), sedentary high-fat diet (HFD, n=5), chow-fed exercise (Exercise, n=5) and HFD-fed exercise (HFD+Exercise, n=5) groups. The exercise groups were subjected to 12 weeks of motorized treadmill running at a speed of 18 m/min for 30 min/day. Differences in post-intervention measures were assessed by analysis of covariance (ANCOVA), adjusted for baseline bodyweight and pre-intervention measures, where available. Post-hoc analyses were performed with Bonferroni correction. Plasma metabolic profile was worsened and fat pads, ectopic fat in muscle and liver and inflammatory markers in skeletal muscle were elevated in sedentary HFD-fed animals relative to chow-fed controls. HFD+Exercise animals had significantly lower leptin (P=0.0004), triglycerides (P=0.007), homeostatic model assessment of insulin resistance (HOMA-IR; P=0.065), intramyocellular lipids (IMCLs; P=0.003), intrahepatic lipids (IHLs; P<0.0001), body fat% (P=0.001), subcutaneous adipose tissue (SAT; P<0.0001), visceral adipose (P<0.0001) and total fat mass (P<0.0001), relative to sedentary HFD-fed animals, despite only modestly lower bodyweight. Messenger RNA (mRNA) expression of inflammatory markers Interleukin 6 (IL6) and Tumor necrosis factor α (TNFα) were also reduced with aerobic exercise in skeletal muscle. Our results suggest that 12 weeks of aerobic exercise training is effective in improving metabolic health, fat depots, ectopic fat and inflammation even against a high-fat dietary background.     

Paternal exercise protects mouse offspring from high-fat-diet-induced type 2 diabetes risk by increasing skeletal muscle insulin signaling

Paternal obesity increases, while paternal exercise decreases, offspring obesity and type 2 diabetes (T2D) risk; however, no studies have determined whether a paternal high-fat (HF) diet and exercise interact to alter offspring body weight (BW), adiposity and T2D risk. Three-week-old male C57BL/6 mice were fed a normal-fat (NF) diet (16% fat) or an HF diet (45% fat) and assigned to either voluntary wheel running exercise or cage activity for 3 months prior to mating with NF-diet-fed dams. After weaning, male offspring were fed an NF or HF diet for an additional 3 months. F1 male mice whose fathers ate an HF diet had decreased % body fat accompanied by decreased gene expression of beige adipocyte marker FGF21. However, paternal HF-diet-induced reductions in F1 offspring % body fat normalized but did not reduce T2D risk. Exercise was protective against paternal HF-diet-induced insulin resistance by increasing the expression of insulin signaling (GLUT4, IRS1 and PI3K) markers in skeletal muscle resulting in normal T2D risk. When fathers were fed an HF diet and exercised, a postnatal HF diet increased beiging (PPARγ). Thus, these findings show that increases in T2D risk in male offspring when the father consumes an HF diet can be normalized when the father also exercises preconception and that this protection may occur by increases in insulin signaling potential within offspring skeletal muscle. Future studies should further determine the physiological mechanism(s) underlying the beneficial effects of exercise through the paternal lineage.     

温度和高脂食物对黑线仓鼠代谢产热和体脂累积的影响

能量代谢的适应性调节是小型哺乳动物应对环境季节性变化的主要策略之一。为探讨不同温度下动物在代谢产热能量支出与脂肪累积之间的权衡策略,以成年雄性黑线仓鼠为研究对象开展了3 个实验:实验1 将动物驯化于高脂和低脂食物;实验2 将动物暴露于低温(5℃)和暖温(30℃);实验3 将饲喂高脂食物的动物暴露于低温。以食物平衡法测定摄食量、摄入能和消化率,以开放式氧气分析仪测定代谢产热,以索氏抽提法测定脂肪含量。结果发现,取食高脂食物的黑线仓鼠摄食量显著减少,但脂肪累积显著增加;暖温下摄食量显著减少,但体脂含量显著增加,低温下摄食量显著升高,但体脂含量显著减少;饲喂高脂食物的黑线仓鼠在低温下摄入能显著增加,非颤抖性产热增强,但体脂含量显著降低。结果表明高脂食物对黑线仓鼠体脂累积的影响与环境温度有关,低温诱导脂肪动员,暖温促进脂肪贮存;低温下黑线仓鼠增加能量摄入不能完全补偿用于产热的能量支出,导致脂肪动员增加;暖温下代谢产热降低是脂肪累积的主要因素;与能量摄入相比代谢产热的能量支出在体脂累积的适应性变化中发挥更重要的作用。     

Improved immune functions with administration of a low-fat diet in a burn animal model

The purpose of this study was to characterize the impact of a low-fat (LF; 1% fat) diet, a high-fat (HF; 25% fat) diet, and a standard (SD; 5% fat) diet on immune and oxidative parameters in a 20% body surface area burn animal model fed ad libitum for 10 days postinjury. Although the mechanisms are poorly understood, the amount of dietary lipid in nutritional support has been shown to have immunomodulatory effects after burn injury. Burned mice fed the LF diet showed a normal response in activated splenocyte proliferation compared to burned animals that received the SD or HF diet. Animals fed the SD and HF diets presented increased production of nitric oxide and prostaglandin E2 response after burn injury, which is associated with inhibited splenocyte proliferation. The total thiol concentration in spleen cells from burned animals kept on the HF diet was significantly higher than that in unburned animals, while no increase in these oxidative parameters was observed in LF-fed burned animals. Moreover, the LF diet significantly reduced hepatic lipid peroxidation, as measured by malonaldehyde concentration, compared to the other two diets. These results suggest that the administration of a LF diet in mice after a burn injury prevents inhibition of in vitro splenocyte proliferation and reduces the intensity of oxidative stress.     

Interactions of dietary fat and 2,5-anhydro-D-mannitol on energy metabolism in isolated rat hepatocytes

The fructose analog 2,5-anhydro-D-mannitol (2,5-AM) stimulates feeding in rats by reducing ATP content in the liver. These behavioral and metabolic effects occur with rats fed a high-carbohydrate/low-fat (HC/LF) diet, but they are prevented or attenuated when the animals eat high-fat/low-carbohydrate (HF/LC) food. To examine the metabolic bases for this effect of diet, we assessed the actions of 2,5-AM on ATP content, oxygen consumption, and substrate oxidation in isolated hepatocytes from rats fed one of the two diets. Compared with cells from rats fed the HC/LF diet ("HC/LF" cells), cells from rats fed the HF/LC diet ("HF/LC" cells) had similar ATP contents but lower oxygen consumption, decreased fructose, and increased palmitate oxidation. 2,5-AM did not decrease ATP content or oxygen consumption in HF/LC cells as much as it did in HC/LF hepatocytes, and it only affected fructose and palmitate oxidation in HC/LF cells. 31P-NMR spectroscopy indicated that differences in phosphate trapping accounted for differences in depletion of ATP by 2,5-AM. These results suggest that intake of the HF/LC diet prevents the eating response and attenuates the decline in liver ATP by shifting hepatocyte metabolism to favor fat over carbohydrate as an energy-yielding substrate.     

Effects of diet quality on energy budgets and thermogenesis in Brandt's voles

Food quality and availability play an important role in an animal's life history. The aim of this study was to examine the effect of diet quality [high-fiber diet (HF) or low-fiber diet (LF)] on energy budgets and thermogenesis in Brandt's voles (Lasiopodomys (Microtus) brandtii). Dry matter intake and gross energy intake increased and digestibility decreased in HF voles compared with LF voles, while the digestible energy intake was similar for both HF and LF voles. Nonshivering thermogenesis (NST) decreased in HF voles, while LF voles kept stable; no significant differences were detected in basal metabolic rate (BMR), BAT uncoupling protein 1 (UCP1) content and the levels of serum thyroid hormones (T3 and T4) between HF and LF voles. Although there were no differences in body fat content and serum leptin concentrations between HF and LF voles, serum leptin concentrations in HF voles were reduced to nearly half as those seen in LF voles after 4-weeks acclimation. These results support the hypothesis that Brandt's voles can compensate the poor quality diet physiologically by the means of increasing food intake and decreasing thermogenesis.     

Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats

Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure (CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well-defined animal model of heart failure (HF), using the lean male spontaneously hypertensive HF (SHHF) rat. In this model, animals typically present with decompensated, dilated HF between approximately 18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise-trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low-intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival (P < 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain (MyHC) isoform shift from alpha- to beta-MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length (approximately 6%), width, and area and prevented the increase in the length-to-width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low-intensity exercise training. No significant alterations in sarco(endo)plasmic reticulum Ca2+ ATPase, phospholamban, or Na+/Ca2+ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low-intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF.     

Energy‐Restricted High‐Fat Diets Only Partially Improve Markers of Systemic and Adipose Tissue Inflammation

This study aimed at investigating whether the weight loss due to energy‐restricted high‐fat diets is accompanied with parallel improvements in metabolic markers and adipose tissue inflammation. Eight‐week‐old C57BL/6J mice were given free access to a low‐fat (LF) or a high‐fat (45% of energy from fat—HF) diet for 6 months. Restricting intake of the HF diet by 30% (HFR) during the last 2 months of the HF feeding trial decreased fasting plasma insulin, homeostasis model assessment of insulin resistance (HOMA_IR), and plasma triglyceride levels and improved hepatic steatosis compared to ad libitum HF feeding, indicating an improved metabolic profile. Further, analysis of gonadal white adipose tissue (GWAT) gene expression by microarray and quantitative PCR analyses demonstrated that HFR downregulated expression of genes linked to cell and focal adhesion, cytokine‐cytokine receptor interaction, and endoplasmic reticulum (ER)–associated degradation pathway. However, HFR had no effect on circulating plasminogen activator inhibitor‐1 (PAI‐1) and nonesterified fatty acid levels, which were persistently higher in both HF and HFR groups compared to the LF group. Furthermore, HFR had a negative effect on plasma total adiponectin level. Finally, while HFR decreased GWAT monocyte chemotactic protein‐1 (MCP‐1), interleukin‐2 (IL‐2), and PAI‐1 levels, it did not affect several other cytokines including granulocyte‐macrophage colony‐stimulating factor, interferon‐γ, IL‐1β, IL‐6, and IL‐10. In summary, energy‐restricted high‐fat diets improve insulin sensitivity, while only partially improving markers of systemic and adipose tissue inflammation. In conclusion, our study supports the recommended low‐fat intake for overall cardiovascular health.     

Exercise improves glucose homeostasis that has been impaired by a high-fat diet by potentiating pancreatic beta-cell function and mass through IRS2 in diabetic rats.

In this study, we investigated the effects of a high-fat diet and exercise on pancreatic beta-cell function and mass and its molecular mechanism in 90% pancreatectomized male rats. The pancreatectomized diabetic rats were given control diets (20% energy) or a high-fat (HF) diet (45% energy) for 12 wk. Half of each group was given regular exercise on an uphill treadmill at 20 m/min for 30 min 5 days/wk. HF diet lowered first-phase insulin secretion with glucose loading, whereas exercise training reversed this decrease. However, second-phase insulin secretion did not differ among the groups. Exercise increased pancreatic beta-cell mass. This resulted from stimulated beta-cell proliferation and reduced apoptosis, which is associated with potentiated insulin or IGF-I signaling through insulin receptor substrate-2 (IRS2) induction. Although the HF diet resulted in decreased proliferation and accelerated apoptosis by weakened insulin and IGF-I signaling from reduction of IRS2 protein, beta-cell mass was maintained in HF rats just as much as in control rats via increased individual beta-cell size and neogenesis from precursor cells. Consistent with the results of beta-cell proliferation, pancreas duodenal homeobox-1 expression increased in the islets of rats in the exercise groups, and it was reduced the most in rats fed the HF diet. In conclusion, exercise combined with a moderate fat diet is a good way to maximize beta-cell function and mass through IRS2 induction to alleviate the diabetic condition. This study suggests that dietary fat contents and exercise modulate beta-cell function and mass to overcome insulin resistance in two different pathways.     

Exercise,but not quercetin,ameliorates inflammation,mitochondrial biogenesis,and lipid metabolism in skeletal muscle after strenuous exercise by high-fat diet mice

[Purpose]

The purpose of this study was to investigate whether moderate exercise and quercetin intake with a low fat diet contribute to inflammatory cytokine production, mitochondrial biogenesis, and lipid metabolism in skeletal muscle after strenuous exercise by high-fat diet mice.

[Methods]

Male C57BL/6 mice were randomly divided into four groups: (1) High-fat for 12 weeks and low-fat diet control (C; n = 6); (2) high-fat diet for 12 weeks and low-fat diet with quercetin (Q; n = 4); (3) high-fat diet for 12 weeks and low-fat diet with exercise (E; n = 4); or (4) high-fat diet for 12 weeks and low-fat diet with exercise and quercetin (EQ; n = 5). Quercetin (10 mg/kg) was administered once per day, 5 day/week for 8 weeks. Exercise training was performed at moderate intensity for 8 weeks, 5 days/week for 30–60 min/day. Mice were subjected to a strenuous exercise bout of 60 min at a speed of 25 m/min (VO₂ max 85%) conducted as an exercise-induced fatigue just before sacrifice.

[Results]

As results, body weights were significantly different among the groups. Exercise training significantly reduced inflammatory cytokines after strenuous exercise in skeletal muscle of high-fat diet mice. Exercise training increased Tfam mRNA in the soleus muscle after strenuous exercise. Exercise training significantly decreased lipogenesis markers in skeletal muscle of obese mice after strenuous exercise. Moderate exercise significantly increased lipolysis markers in the tibialis anterior muscle.

[Conclusion]

These findings suggest that exercise training reduced inflammatory cytokine levels and improved mitochondrial biogenesis and lipid metabolism. However quercetin supplementation did not affect these parameters. Thus, long-term moderate exercise training has positive effects on obesity.     

Growth hormone-mediated breakdown of body fat: insulin and leptin responses to GH are modulated by diet composition and caloric intake in old rats.

This work was performed to elucidate whether growth hormone (GH)-mediated loss of adipose tissue and responses in plasma insulin and leptin are modulated by diet composition. 12-month-old rats were first fed a high-fat (HF) diet or a low-fat (LF) diet for 14 weeks. After that, GH or saline was administered to rat groups that were maintained on either HF or LF diets or that were switched from the HF to the LF diet. All 6 groups had free access to food. One additional saline group was pair-fed with the GH group that was switched from the HF to the LF diet. The caloric consumption of this latter group was also translated to yet another GH group receiving restricted amounts of the HF diet. GH was given in a total dose of 4 mg/kg/d for three weeks. After sacrifice, blood was collected and tissues were excised. In groups injected with saline, the weight of excised adipose tissue was 60 +/- 4.7, 41 +/- 3.8 and 50 +/- 4.5 g in animals that continued with the HF diet, LF diet, or that were switched from HF to LF, respectively. Corresponding figures after GH treatment were significantly (p < 0.05) decreased to 38 +/- 2.7, 30 +/- 2.3, and 31 +/- 2.7 g, respectively. Pair-feeding had no effect, whereas only 26 +/- 3.0 g of adipose tissue was retrieved in rats fed restricted amounts of HF diet while receiving GH. In this group, plasma insulin and leptin were also significantly (p < 0.05) depressed compared with other GH groups, especially to the group fed the unrestricted HF diet (203 +/- 35 vs. 1345 +/- 160 pmol/l and 9.3 +/- 1.2 vs. 31 +/- 4.4 micro g/l). In conclusion, this study shows that GH mediates breakdown of adipose tissue under a variety of dietary conditions, and that induction of hyperinsulinemia can be prevented if GH treatment is combined with restricted feeding of a diet which is relatively low in carbohydrates and rich in fat. This will also promote a fall of plasma leptin.     

Physical exercise mitigates high-fat diet-induced adiposopathy and related endocrine alterations in an animal model of obesity

The dysregulation of adipokine secretion owing to adiposopathy can contribute to the pathogenesis of obesity-related disorders. Being that exercise is an advised strategy against obesity-induced adiposopathy, we aimed to analyze the role of physical exercise as a preventive and therapeutic strategy against high-fat diet (HFD)-induced adipokine and ghrelin alterations. Rats were pair-fed the Lieber De Carli standard diet (S, 35 Kcal% fat) or HFD (71 Kcal% fat) over 17 weeks. Animals were assigned into four groups as follows: standard diet sedentary (SS), standard diet voluntary physical activity (SVPA), high-fat diet sedentary (HS), and high-fat diet voluntary physical activity (HVPA). After 9 weeks of dietary treatment, half of the SS and HS animals were submitted to an 8-week endurance training program, standard diet endurance training (SET), and high-fat-diet endurance training (HET) groups, maintaining the respective diets. Although there were no changes in body weight, HFD increased visceral adiposity, percentage of large adipocytes, hypoxia inducible factor (HIF)-1α, and leptin contents in epididymal adipose tissue (eWAT) and decreased plasma content of adiponectin (AdipQ). Both VPA and ET decreased visceral adiposity and percentage of large adipocytes in HFD-fed animals, but ET also increased the percentage of small- to medium-sized adipocytes. VPA increased plasma growth hormone secretagogue receptor (GHS-R) and decreased leptin protein in HVPA group. ET decreased plasma insulin and leptin levels and eWAT HIF-1α and leptin expression in HET group. Moreover, ET improved insulin sensitivity, plasma high molecular weight, and AdipQ and ghrelin levels and increased eWAT and GHS-R expression. Our data suggest that exercise, particularly ET, reverted adiposopathy and related endocrine alterations induced by an isocaloric HFD pair-fed diet.     

Exercise training is more effective than resveratrol supplementation on alleviation of inflammation in peritoneal macrophages of high fat diet mice

[Purpose]

This study investigated the effect of exercise training and resveratrol supplementation with low fat diet on proinflammatory profiles by Lipopolysaccharide (LPS)-stimulation in peritoneal macrophage of high fat diet mice.

[Methods]

To accomplish the purpose of this study, C57BL/6 male mice were fed high fat diet (45% fat diet) for 8 weeks. Then these mice were divided into 3 groups; HLC (high fat diet and low fat diet for 8 weeks as the control, n=10), HLR (high fat diet and low fat diet for 8 weeks with resveratrol supplementation, n=10). HLE (high fat diet and low fat diet for 8 weeks with moderate exercise training, n=10). Resveratrol (10 mg/kg) was administrated once a day, 5 days/week for 8 weeks. Exercise training was performed for 8 weeks on a treadmill running for 30-60 min/day at 10-22 m/min, 0% grade, 5 days/week. After exercise training, all the peritoneal macrophage was collected and LPS (0, 0.5, 1.0 μg/ml) were used to stimulate the cells. Then peritoneal macrophage TNF-α, IL-6, MCP-1, IL12p70, IFN-γ, IL-10 were measured by BD cytometric bead array mouse inflammation kit.

[Results]

As a result, body weight and total cholesterol were significantly reduced in HLE compared with HLC (p<.05). Also, TNF-α and MCP-1 were decreased in HLE compared with HLC (p<.05) by LPS-stimulation (0, 0.5, 1.0 μg/ml) and IL-6, IL-12p70 and IFN-r were decreased in HLE compared with HLC (p<.05) by LPS-stimulation (1.0 μg/ml). But resveratrol supplementation did not affect the result.

[Conclusion]

These findings suggest that exercise training has beneficial effects on body weight, total cholesterol, peritoneal macrophage and proinflammatory cytokine in high fat diet mice.     

Exercise ameliorates high-fat diet-induced metabolic and vascular dysfunction, and increases adipocyte progenitor cell population in brown adipose tissue

A high-fat diet (HFD) is associated with adipose inflammation, which contributes to key components of metabolic syndrome, including obesity and insulin resistance. The increased visceral adipose tissue mass associated with obesity is the result of hyperplasia and hypertrophy of adipocytes. To investigate the effects of exercise on HFD-induced metabolic disorders, male C57BL/6 mice were divided into four groups: SED (sedentary)-ND (normal diet), EX (exercise)-ND, SED-HFD, and EX-HFD. Exercise was performed on a motorized treadmill at 15 m/min, 40 min/day, and 5 day/wk for 8 wk. Exercise resulted in a decrease in abdominal fat contents and inflammation, improvements in glucose tolerance and insulin resistance, and enhancement of vascular constriction and relaxation responses. Exercise with or without HFD increased putative brown adipocyte progenitor cells in brown adipose tissue compared with groups with the same diet, with an increase in brown adipocyte-specific gene expression in brown and white adipose tissue. Exercise training enhanced in vitro differentiation of the preadipocytes from brown adipose depots into brown adipocytes and enhanced the expression of uncoupling protein 1. These findings suggest that exercise ameliorates high-fat diet-induced metabolic disorders and vascular dysfunction, and increases adipose progenitor cell population in brown adipose tissue, which might thereby contribute to enhanced functional brown adipose.     

Insulin sensitivity linked skeletal muscle Nr4a1 DNA methylation is programmed by the maternal diet and modulated by voluntary exercise in mice

Perinatal maternal high-fat consumption is known to increase the obesity and type 2 diabetes susceptibility and to impair exercise performance in the offspring. We hypothesize that epigenetic modifications in the skeletal muscle are partly responsible for this phenotype. To detect skeletal muscle genes affected by maternal nutrition, male offspring of low-fat (LF) and high-fat (HF) diet fed dams (BL6 mice) received LF diet upon weaning and were sacrificed at 6 or 25 weeks of age. Gene expression of Musculus quadriceps was investigated by microarray analysis revealing an up-regulation of the nuclear receptor Nr4a1 by maternal HF feeding. This was accompanied by promoter hypomethylation of CpG_-1408 which correlated with increased Nr4a1 gene expression at both ages. Offspring voluntary exercise training (by supplying running wheels from 7 to 25 weeks of age) normalized Nr4a1 methylation and gene expression respectively, and ameliorated the negative effects of maternal HF feeding on insulin sensitivity. Overall, Nr4a1 gene expression in skeletal muscle correlated with higher insulin levels during an oral glucose tolerance test and could, therefore, be involved in programming type 2 diabetes susceptibility in offspring exposed to perinatal high fat diet.