Effects of high-fat diet and exercise training on intracellular glucose metabolism in rats

We examined the effects of high-fat diet (HFD) and exercise training on insulin-stimulated whole body glucose fluxes and several key steps of glucose metabolism in skeletal muscle. Rats were maintained for 3 wk on either low-fat (LFD) or high-fat diet with or without exercise training (swimming for 3 h per day). After the 3-wk diet/exercise treatments, animals underwent hyperinsulinemic euglycemic clamp experiments for measurements of insulin-stimulated whole body glucose fluxes. In addition, muscle samples were taken at the end of the clamps for measurements of glucose 6-phosphate (G-6-P) and GLUT-4 protein contents, hexokinase, and glycogen synthase (GS) activities. Insulin-stimulated glucose uptake was decreased by HFD and increased by exercise training (P < 0.01 for both). The opposite effects of HFD and exercise training on insulin-stimulated glucose uptake were associated with similar increases in muscle G-6-P levels (P < 0.05 for both). However, the increase in G-6-P level was accompanied by decreased GS activity without changes in GLUT-4 protein content and hexokinase activities in the HFD group. In contrast, the increase in G-6-P level in the exercise-trained group was accompanied by increased GLUT-4 protein content and hexokinase II (cytosolic) and GS activities. These results suggest that HFD and exercise training affect insulin sensitivity by acting predominantly on different steps of intracellular glucose metabolism. High-fat feeding appears to induce insulin resistance by affecting predominantly steps distal to G-6-P (e.g., glycolysis and glycogen synthesis). Exercise training affected multiple steps of glucose metabolism both proximal and distal to G-6-P. However, increased muscle G-6-P levels in the face of increased glucose metabolic fluxes suggest that the effect of exercise training is quantitatively more prominent on the steps proximal to G-6-P (i.e., glucose transport and phosphorylation).     

The effects of diet on muscle pH and metabolism during high intensity exercise

Five healthy male subjects exercised for 3 min at a workload equivalent to 100% VO2max on two separate occasions. Each exercise test was performed on an electrically braked cycle ergometer after a four-day period of dietary manipulation. During each of these periods subjects consumed either a low carbohydrate (3 +/- 0%, mean +/- SD), high fat (73 +/- 2%), high protein (24 +/- 3%) diet (FP) or a high carbohydrate (82 +/- 1%), low fat (8 +/- 1%) low protein (10 +/- 1%) diet (CHO). The diets were isoenergetic and were assigned in a randomised manner. Muscle biopsy samples (Vastus lateralis) were taken at rest prior to dietary manipulation, immediately prior to exercise and immediately post-exercise for measurement of pH, glycogen, glucose 6-phosphate, fructose 1,6-diphosphate, triose phosphates, lactate and glutamine content. Blood acid-base status and selected metabolites were measured in arterialised venous samples at rest prior to dietary manipulation, immediately prior to exercise and at pre-determined intervals during the post-exercise period. There was no differences between the two treatments in blood acid-base status at rest prior to dietary manipulation; immediately prior to exercise plasma pH (p less than 0.01), blood PCO2 (p less than 0.01), plasma bicarbonate (p less than 0.001) and blood base-excess (p less than 0.001) values were all lower on the FP treatment. There were no major differences in blood acid-base variables between the two diets during the post-exercise period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of high-intensity exercise and high-fat diet on lipid metabolism in the liver of rats

[Purpose]

This study investigated the effects of high-intensity exercise (Ex) and high dietary fat intake on lipid metabolism in the liver of rats.

[Methods]

Male Sprague-Dawley rats were randomly assigned to one of the four groups (n=10 per group) that were maintained on a normal diet (ND) or high-fat diet (HFD) consisting of 30% fat (w/w), with or without exercise on a treadmill at 30 m/min and 8% grade) for 4 weeks (i.e., ND, ND+Ex, HFD, and HFD+Ex groups).

[Results]

Body weight (p<.001), total plasma cholesterol (TC) (p<.001), triglyceride (TG) (p<.05), and liver TG levels (p<.05) were increased in the HFD group relative to the ND groups, and serum glucose (p<.05), insulin (p<.05), homeostatic model assessment of insulin resistance (HOMA-IR) (p<.01), and liver TG levels (p<.01) were also higher in the HFD group compared to the ND+Ex group. Plasma free fatty acid was elevated in the HFD+Ex group compared to the HFD group (p<.01). With the exception of acetyl coenzyme A carboxylase, the expression of lipid metabolism-related genes in the liver was altered in the Ex groups compared to the control group (p<.05), with genes involved in lipolysis specifically up regulated in the HFD+Ex group compared to the other groups.

[Conclusion]

Vigorous exercise may increase glucose utilization and fat oxidation by activating genes in the liver that are associated with lipid metabolism compared to that in animals consuming a HFD without exercise. Therefore, high intensity exercise can be considered to counter the adverse effects of high dietary fat intake.     

High-fat diet overrules the effects of training on fiber-specific intramyocellular lipid utilization during exercise

In this study, we compared the effects of endurance training in the fasted state (F) vs. the fed state [ample carbohydrate intake (CHO)] on exercise-induced intramyocellular lipid (IMCL) and glycogen utilization during a 6-wk period of a hypercaloric (～+30% kcal/day) fat-rich diet (HFD; 50% of kcal). Healthy male volunteers (18-25 yrs) received a HFD in conjunction with endurance training (four times, 60-90 min/wk) either in F (n = 10) or with CHO before and during exercise sessions (n = 10). The control group (n = 7) received a HFD without training and increased body weight by ～3 kg (P < 0.001). Before and after a HFD, the subjects performed a 2-h constant-load bicycle exercise test in F at ～70% maximal oxygen uptake rate. A HFD, both in the absence (F) or presence (CHO) of training, elevated basal IMCL content by ～50% in type I and by ～75% in type IIa fibers (P < 0.05). Independent of training in F or CHO, a HFD, as such, stimulated exercise-induced net IMCL breakdown by approximately twofold in type I and by approximately fourfold in type IIa fibers. Furthermore, exercise-induced net muscle glycogen breakdown was not significantly affected by a HFD. It is concluded that a HFD stimulates net IMCL degradation by increasing basal IMCL content during exercise in type I and especially IIa fibers. Furthermore, a hypercaloric HFD provides adequate amounts of carbohydrates to maintain high muscle glycogen content during training and does not impair exercise-induced muscle glycogen breakdown.     

Metabolism of substrates: energy substrate metabolism during exercise and as modified by training

The question of what is the source of fuel for oxidation by muscle during exercise has been addressed. A review of experiments spanning more than 60 years supports the concept that the major energy source for the metabolism of exercise is the oxidation of fats and carbohydrates. The relative contribution of these major substrates to the total body metabolism depends on factors such as the intensity and duration of the exercise, the diet consumed on the days before the exercise, and the state of physical training. With light prolonged exercise there is a progressively greater use of fat until it can contribute up to 80% of the total caloric expenditure. However, the relative contribution of fat to the metabolism is less and that of carbohydrate greater as exercise intensity increases. Consumption of a diet rich in fat and protein produces a shift toward a greater use of fat with a concomitant reduction of both the intensity and duration of effort that can be sustained. Conversely, ingestion of a carbohydrate-rich diet increases the percentage of carbohydrate used and increases endurance. The concentration of glycogen in muscle is reduced by fat-protein diets and elevated by carbohydrate-rich diets. Endurance training results in a shift of the metabolism toward a greater use of fat during the same absolute and relative exercise loads. This produces a glycogen sparing that is associated with improving endurance capacity.     

Influence of sex, high-fat diet, and exercise training on potassium currents of swine coronary smooth muscle

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 (I(K)) 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 I(K): 4-aminopyridine-sensitive I(K(KV)), TEA-sensitive I(K(BK)), and 4-aminopyridine + TEA-insensitive I(K). Females exhibited significantly higher basal I(K) than males in the same group. EX increased basal I(K) in males and females. HF reduced I(K) in males and females and nullified effects of EX. Endothelin-1 increased I(K) significantly in males but not in females. In the presence of endothelin-1, 1) I(K(KV)) was similar in SED males and females and EX increased I(K(KV)) to a greater extent in males than in females and 2) I(K(BK)) was greater in SED females than in males and EX increased I(K(BK)) to a greater extent in males, resulting in I(K(BK)) similar to EX females. Importantly, HF nullified effects of EX on I(K(KV)) and I(K(BK)). These data indicate that basal I(K) of SED female swine is inherently greater than that shown in SED males and that males require EX to achieve comparable levels of I(K). Importantly, HF reduced I(K) in males and females and nullified effects of EX, suggesting HF abrogates beneficial effects of EX on coronary smooth muscle.     

Effect of endurance training on gross energy expenditure during exercise

We compared the effect of endurance exercise training on gross energy expenditure (GEE) during steady-state exercise in 20 younger men (31.2 +/- 0.6 years) and 20 middle-aged men (49.2 +/- 1.1 years). The subjects trained for eight months. The training program consisted of three 45-min walking and jogging exercise sessions per week at an intensity of approximately 60-85% of the heart rate at peak VO2. We administered bicycle ergometer tests at 0, 4, and 8 months into training. Participants exercised at a power output of 100 W for 10 min using a pedaling frequency of 50 rpm. We determined GEE (kcal/min) by measuring the oxygen consumption and respiratory exchange ratio. We found a significant reduction (p less than 0.05) in GEE (0.7-1.3 kcal/min) following 4 months of endurance training in both age groups, with a further reduction (p less than 0.05) noted in only the middle-aged group at month 8. We found no difference (p greater than 0.05) in GEE between the younger and middle-aged men. We conclude that chronic exercise may modify GEE during a submaximal exercise bout and that this adaptation is similar in magnitude in younger and middle-aged men.     

Effects of angiotensin II AT1 receptor inhibition and exercise training on insulin action in rats on high-fat diet

AimThis study was to determine whether combination of the angiotensin II AT1 receptor blocker (ARB), candesartan cilexetil, and exercise training can prevent the development of high-fat diet-induced insulin resistance.Main methodsF344/NSlc rats were fed normal chow diet or high-fat (HF) diet for 7 weeks. The HF-fed rats were either administered candesartan cilexetil (5 mg·kg^? 1·day^? 1), exercise-trained, or received a combination of these 2 treatments.Key findingsOral glucose tolerance tests (OGTT) showed that combined treatment with candesartan cilexetil and exercise increased glucose tolerance as compared with each treatment alone in HF-fed rats. Moreover, euglycemic–hyperinsulinemic clamp analysis showed improvement in glucose infusion rate with exercise training or candesartan cilexetil treatment alone, and further improvement was observed with the combination treatment. Systolic blood pressure improved with candesartan cilexetil but not with exercise alone. Finally, Glut-4 protein expression in soleus muscle was decreased with HF diet, and the expression was increased by exercise and not candesartan cilexetil treatment.SignificanceThese results suggest that the combination of candesartan cilexetil and exercise training improves insulin resistance as compared with each treatment alone.     

Differential effects of short- and long-term high-fat diet feeding on hepatic fatty acid metabolism in rats

Imbalance in the supply and utilization of fatty acids (FA) is thought to contribute to intrahepatic lipid (IHL) accumulation in obesity. The aim of this study was to determine the time course of changes in the liver capacity to oxidize and store FA in response to high-fat diet (HFD). Adult male Wistar rats were fed either normal chow or HFD for 2.5weeks (short-term) and 25weeks (long-term). Short-term HFD feeding led to a 10% higher palmitoyl-l-carnitine-driven ADP-stimulated (state 3) oxygen consumption rate in isolated liver mitochondria indicating up-regulation of β-oxidation. This adaptation was insufficient to cope with the dietary FA overload, as indicated by accumulation of long-chain acylcarnitines, depletion of free carnitine and increase in FA content in the liver, reflecting IHL accumulation. The latter was confirmed by in vivo((1))H magnetic resonance spectroscopy and Oil Red O staining. Long-term HFD feeding caused further up-regulation of mitochondrial β-oxidation (24% higher oxygen consumption rate in state 3 with palmitoyl-l-carnitine as substrate) and stimulation of mitochondrial biogenesis as indicated by 62% higher mitochondrial DNA copy number compared to controls. These adaptations were paralleled by a partial restoration of free carnitine levels and a decrease in long-chain acylcarnitine content. Nevertheless, there was a further increase in IHL content, accompanied by accumulation of lipid peroxidation and protein oxidation products. In conclusion, partially effective adaption of hepatic FA metabolism to long-term HFD feeding came at a price of increased oxidative stress, caused by a combination of higher FA oxidation capacity and oversupply of FA.     

Combination of meal and exercise timing with a high-fat diet influences energy expenditure and obesity in mice

In mice, obesity has been observed not only in those freely fed a high-fat diet (HFD) but also in those fed while physically inactive. In contrast, a HFD during physically active periods protects against obesity and the impairments in the circadian rhythm induced by free feeding of a HFD. Although exercise is known to be effective for obesity prevention and management, the optimal timing of exercise has not yet been determined. In the present experiments, we aimed to determine the best combination of daily timing of HFD consumption and exercise for the prevention of HFD-induced weight gain in mice. In this experiment, “morning” refers to the beginning of the active phase (the “morning” for nocturnal animals). Increases in body weight related to free feeding of a HFD was significantly reduced with 4?h of exercise during the late (evening) or middle (noon) active period compared to 4?h of exercise during the early (morning) active period or free access to exercise, which resulted in hours of exercise similar to that of morning exercise. These results suggested that eating in the morning or at noon followed by exercise in the evening could prevent weight gain more effectively than exercise in the morning followed by eating at noon or in the evening. The group fed a HFD for 4?h in the morning had lower body weight than the group fed a HFD for 4?h in the evening without exercise. The last group of experiments tested the hypothesis that there would be an interaction between mealtime and exercise time (i.e. time of day) versus order (i.e. which comes first) effects. We compared groups that exercised for 4?h at noon and were fed either in the morning or evening and groups that were fed for 4?h at noon and either exercised in the morning or evening. We found that the groups that were fed before exercise gained less body and fat weight and more skeletal muscle weight compared to the groups that exercised before eating. Corresponding to the body and fat weight changes, the respiratory exchange ratio (RER) was lower and energy expenditure was higher in the groups fed before exercise than in the groups fed after exercise, and these effects on energy metabolism were also observed in the early stage of HFD feeding before obesity. When obese mice fed a HFD for 12 weeks were exposed to a combination of feeding and exercise timing in an effort to reduce body weight, eating followed by exercise resulted in greater weight loss, similar to the experiments conducted to prevent weight gain. These results demonstrate that a combination of daily timing of eating and exercise may influence weight gain and that eating followed by exercise may be effective for minimizing increases in body and fat weight as well as maximizing increases in skeletal muscle weight.     

Effects of diet and exercise on metabolic disturbances in high-fat diet-fed mice

Consumption of a high-fat diet (HFD) is associated with white adipose tissue (WAT) inflammation, which contributes to key components of the metabolic syndrome, including insulin resistance (IR) and hepatic steatosis (HS). To determine the differential effects of exercise training (EX), low-fat diet (LFD), and their combination on WAT inflammation, Balb/cByJ male mice (n = 34) were fed an HFD for 12 wks before they were randomized into one of four intervention groups: HFD-EX, LFD-EX, HFD-sedentary (SED), or LFD-SED. EX mice performed 12 wks of exercise training on a motorized treadmill (1 h/d, 5 d/wk, 12 m/min, 5% grade, 65% VO₂ max), while SED mice remained sedentary in their home cages. WAT gene expression of adipokines was assessed using rt-PCR. IR was measured using HOMA-IR, and HS via hepatic triglyceride content. EX significantly reduced (53%) WAT gene expression of MCP-1, and LFD significantly reduced (50%) WAT gene expression of the macrophage specific marker, F4/80 as well as the adipocytokine IL-1ra (25%). EX independently improved IR, while both EX and LFD improved HS. These findings suggest that both diet and exercise have unique beneficial effects on WAT inflammatory markers and the mechanism by which each treatment improves metabolic complications associated with chronic consumption of an HFD may be different.     

Betaine supplementation prevents fatty liver induced by a high-fat diet: effects on one-carbon metabolism

The purpose of this study was to examine the effects of betaine supplementation on the regulation of one-carbon metabolism and liver lipid accumulation induced by a high-fat diet in rats. Rats were fed one of three different liquid diets: control diet, high-fat diet and high-fat diet supplemented with betaine. The control and high-fat liquid diets contained, respectively, 35 and 71 % of energy derived from fat. Betaine supplementation involved the addition of 1 % (g/L) to the diet. After three weeks on the high-fat diet the rats had increased total liver fat concentration, liver triglycerides, liver TBARS and plasma TNF-α. The high-fat diet decreased the hepatic S-adenosylmethionine concentration and the S-adenosylmethionine/S-adenosylhomocysteine ratio compared to the control as well as altering the expression of genes involved in one-carbon metabolism. Betaine supplementation substantially increased the hepatic S-adenosylmethionine concentration (~fourfold) and prevented fatty liver and hepatic injury induced by the high-fat diet. It was accompanied by the normalization of the gene expression of BHMT, GNMT and MGAT, which code for key enzymes of one-carbon metabolism related to liver fat accumulation. In conclusion, the regulation of the expression of MGAT by betaine supplementation provides an additional and novel mechanism by which betaine supplementation regulates lipid metabolism and prevents accumulation of fat in the liver.     

Age and aerobic exercise training effects on whole body and muscle protein metabolism

Aging in humans is associated with loss of lean body mass, but the causes are incompletely defined. Lean tissue mass and function depend on continuous rebuilding of proteins. We tested the hypotheses that whole body and mixed muscle protein metabolism declines with age in men and women and that aerobic exercise training would partly reverse this decline. Seventy-eight healthy, previously untrained men and women aged 19-87 yr were studied before and after 4 mo of bicycle training (up to 45 min at 80% peak heart rate, 3-4 days/wk) or control (flexibility) activity. At the whole body level, protein breakdown (measured as [13C]leucine and [15N]phenylalanine flux), Leu oxidation, and protein synthesis (nonoxidative Leu disposal) declined with age at a rate of 4-5% per decade (P < 0.001). Fat-free mass was closely correlated with protein turnover and declined 3% per decade (P < 0.001), but even after covariate adjustment for fat-free mass, the decline in protein turnover with age remained significant. There were no differences between men and women after adjustment for fat-free mass. Mixed muscle protein synthesis also declined with age 3.5% per decade (P < 0.05). Exercise training improved aerobic capacity 9% overall (P < 0.01), and mixed muscle protein synthesis increased 22% (P < 0.05), with no effect of age on the training response for either variable. Fat-free mass, whole body protein turnover, and resting metabolic rate were unchanged by training. We conclude that rates of whole body and muscle protein metabolism decline with age in men and women, thus indicating that there is a progressive decline in the body's remodeling processes with aging. This study also demonstrates that aerobic exercise can enhance muscle protein synthesis irrespective of age.     

Effect of chronic consumption of a high-fat diet on mammary metabolism

Rats have been fed semi-synthetic diets containing 4 and 20% (w/w) corn oil for periods of 9-12 weeks covering two lactations. The mean maternal and pup weights at day-14 of the second lactation on the diets were not significantly different. The milk fatty acids of the rats on the high-fat diet contained 39 mol% linoleic acid and only 20 mol% medium-chain acids compared with over 40% for the low-fat diet. With the exception of "malic" enzyme, none of five enzymes assayed in mammary supernatants was significantly altered by the diet fed. These results suggest that the synthesis of these enzymes in the mammary gland is insensitive to dietary lipid.     

Impact of high-fat diet and obesity on energy balance and fuel utilization during the metabolic challenge of lactation

The effects of obesity and a high-fat (HF) diet on whole body and tissue-specific metabolism of lactating dams and their offspring were examined in C57/B6 mice. Female mice were fed low-fat (LF) or HF diets before and throughout pregnancy and lactation. HF-fed mice were segregated into lean (HF-Ln) and obese (HF-Ob) groups before pregnancy by their weight gain response. Compared to LF-Ln dams, HF-Ln, and HF-Ob dams exhibited a greater positive energy balance (EB) and increased dietary fat retention in peripheral tissues (P < 0.05). HF-Ob dams had greater dietary fat retention in liver and adipose compared to HF-Ln dams (P < 0.05). De novo synthesized fat was decreased in tissues and milk from HF-fed dams compared to LF-Ln dams (P < 0.05). However, less dietary and de novo synthesized fat was found in the HF-Ob mammary glands compared to HF-Ln (P < 0.05). Obesity was associated with reduced milk triglycerides relative to lean controls (P < 0.05). Compared to HF diet alone obesity has additional adverse affects, impairing both lipid metabolism as well as milk fat production. Growth rates of LF-Ln litters were lower than HF-Ln and HF-Ob litters (P < 0.05). Total energy expenditure (TEE) of HF-Ob litters was reduced relative to HF-Ln litters, whereas their respiratory exchange ratios (RERs) were increased (P < 0.05). Collectively these data show that consumption of a HF diet significantly affects maternal and neonatal metabolism and that maternal obesity can independently alter these responses.     

Effects of a high-fat diet on energy intake and expenditure in rats

The effects of a high-fat diet supplying a constant energy/protein ratio, with and without overeating, on energy intake and expenditure was studied in mature male rats. A control group (LF) received $\text{ad libitum}$ access to a low-fat diet. Body weight gain, efficiency of food utilization, and dietary-induced thermogenesis were increased relative to controls in a group with $\text{ad libitum}$ access to the high-fat diet (HF-A), but not in a group which was pair fed the diet (HF-P) in amounts (kcal) equal to that of LF animals. However, the individual variability within the HF-A group was high for each measure. An arbitrary separation of that group into 2 subgroups (based on high vs low weight gain) produced one subgroup with increased efficiency, greater weight gain and no change in dietary-induced thermogenesis (HF-AH), and another with no difference in efficiency or in weight gain from the LF group but which had higher dietary-induced thermogenesis (HF-AL). Food intake was slightly, but not significantly, greater for the HF-AH subgroup than for the HF-AL subgroup. We conclude that rats can increase thermogenesis in response to overeating but that the increase is highly variable. The thermogenic response appears to be related to the overeating rather than to the fat content of the diet.     

Resveratrol treatment improves the altered metabolism and related dysbiosis of gut programed by prenatal high-fat diet and postnatal high-fat diet exposure

A maternal high-fat (HF) diet sensitizes offspring to the adverse effects of postnatal HF intake and can lead to metabolic dysregulation. Resveratrol, a natural polyphenolic compound found in grapes and red wine, could help to relieve metabolic syndrome dysregulation. Since the gut microbiota is known to be closely related to metabolic homeostasis, this study aimed to investigate the impact of a combination of maternal and postweaning HF diets on the gut microbiota and whether resveratrol could relieve the gut dysbiosis associated with metabolic dysregulation. Sprague–Dawley dams were sustained on either a chow or HF diet before mating, during pregnancy and during lactation. Their offspring were randomly fed chow or a HF diet after weaning. Four experimental groups were generated: CC (maternal/postnatal chow diet), HC (maternal HF/postnatal chow diet), CH (maternal chow/postnatal high-fat diet) and HH (maternal/postnatal HF diet). A fifth group consisted of HH with resveratrol treatment. We found that both maternal and postnatal HF exposure has a distinct effect on the gut microbiota metagenome of offspring. Maternal HF diet exposure decreased plasma acetate, propionate and butyrate level, while postnatal HF diet exposure decreased plasma acetate level in adult life. The metabolic dysregulation programed by the maternal and postnatal HF diets was related to the relevant gut microbiota. Resveratrol treatment ameliorated the altered plasma propionate level related to maternal HF and postnatal HF diet treatment. Resveratrol treatment also improved most of the altered metabolic dysregulation and related dysbiosis programmed by maternal and postnatal HF diet exposure.     

有氧运动联合黑果枸杞对高脂膳食大鼠心肌脂代谢某些指标的影响

目的:研究有氧运动联合黑果枸杞对高脂膳食大鼠心肌脂代谢某些指标的影响。方法:55只雄性Wistar大鼠经过适应性饲养4 d后进行20 min/d的无负重游泳训练,连续3 d,筛选淘汰5只不适应游泳训练的大鼠后,按体重以数字随机分组法分为5组:普通膳食+安静组(RDC组)、高脂膳食+安静组(HDC组)、高脂膳食+黑果枸杞+安静组(HDLC组)、高脂膳食+有氧运动组(HDM组)、高脂膳食+黑果枸杞+有氧运动组(HDLM),每组10只。HDM组和HDLM组进行6周每周6次60 min/d的无负重游泳训练。RDC组大鼠以普通饲料常规喂养;其余各组以高脂饲料喂养; HDLC组和HDLM组大鼠灌胃黑果枸杞,灌胃剂量为4.48 g/(kg·d),灌胃体积为5 ml/kg,其余各组灌胃等量蒸馏水。6周后,测定大鼠Lee’s指数,取血、心肌检测相关生化指标。结果:与RDC组比较,HDC组Lee’s指数,血清FFA、TNF-α、IL-6、TC、TG、LDL-C,心肌FFA、ICAM-1显著升高(P<0.01);血清HDL-C水平显著降低(P<0.01)。与HDC组比较,HDLC、HDM、HDL...