Exercise improves high fat diet-impaired vascular function

  • Authors:
    • Jun Fang
    • Mei Tang
  • View Affiliations

  • Published online on: August 25, 2017     https://doi.org/10.3892/br.2017.972
  • Pages: 337-342
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The prevalence of metabolic syndrome and cardiovascular disease is increasing due to increases in the consumption of high fat diets (HFDs) and the epidemic of obesity. In the present study, it was hypothesized that swimming exercise may prevent HFD-induced impairment of aortic function and that these changes are associated with reduction of oxidative stress, proinflammatory adipokines/cytokines. Male, 6-week-old C57BL/6J mice were fed a 60% lipid composition HFD with or without swimming exercise (90 min/swim and 2 swims/day) for 16 weeks. Exercise training prevented HFD-induced increases in visceral fat weight, total cholesterol and triglycerides. Furthermore, exercise training improved HFD-impaired aortic endothelium-dependent dilation that was associated with reduction of oxidative stress, leptin, resistin, monocyte chemoattractant protein 1, interleukin (IL)6 and IL8. In addition, exercise inhibited HFD-induced vascular endothelial growth factor expression in gastrocnemius skeletal muscle. These data demonstrate that swimming exercise prevents aortic tissue oxidative stress, inflammation and vascular dysfunction in HFD-induced obesity.


The rising prevalence of obesity is associated with an increase in the consumption of high fat diets (HFDs), which contributes to early structural alterations and increases the risk for cardiovascular disease (CVD)-associated morbidity and mortality (1,2). Thus, obesity-induced vascular impairment is markedly associated with damage to target organs, including the heart, kidney, liver and brain (3). For example, aortic relaxation dysfunction, a type of vascular dysfunction, decreases diastolic pressure and increases systolic pressure, which increases cardiac afterload, left ventricular mass and cardiac oxygen demand (4). In addition, the decrease in diastolic pressure contributes to reduction of coronary blood flow in the period of cardiac diastole (4). Factors, such as increased reactive oxygen species (ROS), release of proinflammatory apipokines/cytokines, and tissue insulin resistance are involved in the abnormal vascular pathophysiological changes and associated CVD (5). The combination of abnormal eating habits and a sedentary lifestyle increase the risk factors of obesity and CVD (6). A previous study has demonstrated that exercise improves vascular function by increasing the vascular mitochondrial respiratory capacity, bioavailable nitric oxide (NO), and redox balance in a sedentary rodent model (7). While prolonged sitting in humans prompts leg endothelial dysfunction, fidgeting improves leg endothelial and vascular function through the intermittent increases in vascular shear stress (8). Thus, the underlying mechanisms and interactions between obesity and exercise in the regulation of vascular function involve a complicated network of interacting factors that require investigation. Therefore, the present study hypothesized that HFD-induced vascular dysfunction is mediated by dyslipidemia, excessive ROS, increased expression levels of proinflammatory adipokines and maladaptive immune responses, and these abnormalities are prevented by swimming exercise. An improved understanding of the underlying mechanisms of vascular function obesity and exercise will be of great clinical significance.

Materials and methods


A total of 21 male, 6-week-old C57BL/6J mice were purchased from the Beijing HFK Bioscience Co., Ltd. (Beijing, China). For the obese and exercise studies, C57BL/6J male mice were fed a 60% lipid composition HFD with or without swimming exercise (90 min/swim and 2 swims/day) for 16 weeks. The control group mice were age-matched, male mice and were fed regular mouse chow during the same period of time. The mice were ~18 g and individually housed on a 12-h light/dark cycle (6 a.m., lights on and 6 p.m., lights off). The laboratory temperature was 24°C and the humidity was 20.5±3.0%. All of the animal studies and procedures were performed in accordance with the Animal Use and Care Committee at the Xianning Central Hospital and The First Clinical Hospital of Hubei University of Science and Technology (Xianning, China). Following completion of the experiments, the mouse aortae were isolated to investigate the vascular activity and the left aortae were maintained in a freezer at −80°C.

Plasma lipid profile assays

During blood sample collection, mice underwent terminal anesthesia, 0.5 ml was collected through cardiac puncture. After the blood was prepared in the heparin-coated tubes, plasma was collected by centrifugation at 604 × g for 15 min. The plasma levels of triglycerides (TG), total cholesterol (TC) and high-density lipoprotein (HDL) were examined using a plasma lipid profile kit (cat. no. MAK043; Sigma-Aldrich; Merck KGaA, Darmstadt, Germany) according to manufacturer's instructions. Serum leptin, resistin and adiponectin levels were measured using a mouse serum adipokine milliplex kit (cat. no. MADKMAG-71K; Shanghai Biotechnology Co., Ltd., Shanghai, China) according to manufacturer's instructions.

Aortic oxidative stress

The formation of ROS in the aortae was evaluated by chemiluminescence. Aortae were homogenized in a glass homogenizer with sucrose buffer (pH 7.5 protease inhibitor tablet, 0.5 mm EDTA, 50 mm HEPES and 250 mm sucrose) (9). The homogenates were centrifuged at 1,500 × g for 10 min at 4°C. Supernatants in the whole homogenate were removed and added to 1.4 ml 50-mm phosphate (KH2PO4) buffer (100 µm NADPH, 1 mm EGTA, 5 µm lucigenin and 150 mm sucrose) for incubation at room temperature for 1 h in dark-adapt counting vials (9). Following dark adaptation, samples were placed in a scintillation counter to count every 30 sec for 10 min using a spectrophotometer (wavelength, 450 nm) and normalized to total protein in the whole homogenate. The ROS values were taken as counts per min per milligram (cpm/mg) of protein (9).

Analysis of vascular function

The thoracic aorta was dissected and sliced in 2 mm long aortic rings that were suspended in 95% O2/5% CO2 aerated organ chambers filled with modified Krebs-Ringer bicarbonate solution (118 mM NaCl, 1.2 mM MgCl2, 4.7 mM KCl, 11.2 mM NaH2PO4, 2.5 mM CaCl2, 1.2 mM Na2SO4, 25 mM NaHCO3, 10 mM glucose; pH 7.4; Sigma-Aldrich; Merck KGaA) (10). Aortic contractile state was ascertained by KCl (80 mM). Rings were pre-constricted with norepinephrine and relaxations to acetylcholine (Ach, 10−9-10−4 M) or sodium nitroprusside (SNP; 10−9-10−4 M; Sigma-Aldrich; Merck KGaA) were obtained in a cumulative fashion.

Western blot analysis

After the mice were under deep anesthesia with sodium pentobarbital (50 mg/kg) intraperitoneal injection, a scalpel cut through the skin all around and just above the ankle, the gastrocnemius muscles were removed from mouse hind limbs and lysed with protein lysis buffer (Sigma-Aldrich; Merck KGaA). After the protein concentration of the lysate was determined by Bio-Rad protein assay (Bio-Rad Laboratories Ltd., Shanghai, China). The proteins (20 µg) were separated on 10% SDS-PAGE gels and transferred onto nitrocellulose membranes at 90 V for 90 min (Sigma-Aldrich; Merck KGaA). Membranes were incubated overnight at 4°C with blocking solution containing antibodies targeting vascular endothelial growth factor (VEGF; cat. no. 07-1420, 1:1,000 dilution; Sigma-Aldrich; Merck KGaA). The membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibody (cat. no. A9542, 1:5,000 dilution; Sigma-Aldrich; Merck KGaA) at room temperature for 1 h. The HRP activity was detected using an enhanced chemiluminescence kit (cat. no. 1705060; Bio-Rad Laboratories Ltd.). GAPDH was run in parallel and served as a loading control.

Reverse transcription-quantitative polymerase chain reaction (RT-qPCR)

The genes associated with expression of pro-inflammatory cytokines were examined by (RT-qPCR) (11). Total RNA was isolated from the aortae using RNAzol (Sigma-Aldrich; Merck KGaA) and cDNA synthesis was completed by using 1 µg total RNA with 5X reaction buffer, oligo(dT) (1 µg), RNAse inhibitor, MgCl2, dNTP mix, and ImProm II reverse transcriptase as per the ImProm II reverse transcription kit (cat. no. 11939823001; Sigma-Aldrich; Merck KGaA). Following first strand cDNA synthesis, qPCR was performed using 8 µl cDNA, 10 µl SYBR-Green PCR master mix (Sigma-Aldrich; Merck KGaA) and forward and reverse primers (10 pM/µl; Sigma-Aldrich; Merck KGaA) using a real-time PCR system (CFX96; Bio-Rad Laboratories, Inc., Hercules, CA, USA). The following primer sequences were used: Forward, 5′-GCGATAGTTAATGCAACACT-3′ and reverse, 5′-TTGGTTACCGGGTGCAGCAC-3′ for monocyte chemoattractant protein 1 (MCP1); forward, 5′-ACACAGTGTGCTCACGCATGA-3′ and reverse, 5′-GCAAAGTTATATGCCGACAGC-3′ for interleukin (IL)6; forward, 5′-CGGAATTGGGGTTCATTTGT-3′ and reverse, 5′-ACTTGCAGTCCGATGCAAGC-3′ for IL8; forward, 5′-GGTAATTAACGCCAAGTCTGA-3′ and reverse, 5′-TGGTCAGCCTAGCTGAGGA-3′ for 18S. The PCR cycling conditions for the gene expression were as follows: 5 min at 95°C for initial denaturation, 39 cycles of 30 sec at 95°C, 30 sec at 58°C and 30 sec at 72°C. The qPCR data were obtained from five different samples in triplicate. Calculations of relative normalized gene expression were performed according to the ΔCt method as described before (7). The data were normalized to housekeeping gene, 18S ribosomal RNA.

Statistical analysis

All data are reported as the mean ± standard error. Statistical analysis was performed using one-way analysis of variance (ANOVA) and analyzed variance using the IBM software SPSS v22.0 (IBM Corp., Armonk, NY, USA). P<0.05 was considered to indicate a statistically significant difference.


Effect of HFD and exercise on body weight, visceral fat weight and plasma lipid profiles

As hypothesized, HFD induced a 2.75-fold increase in body weight, an ~3.5-fold increase in visceral fat body weight compared with the control C57BL/6J mice that were fed regular mouse chow (P<0.05; Table I). The levels of plasma TC and TG were higher in the HFD group than those mice fed with regular mouse chow. However, swimming exercise prevented HFD-induced increases in visceral fat weight, plasma TC and TG levels (Table I). Notably, no significant difference in body weight was noted between HFD alone and HFD with exercise. In addition, no significant difference in HDL level was observed between the three groups of mice.

Table I.

Effects of exercise on characteristics of mice fed with a HFD.

Table I.

Effects of exercise on characteristics of mice fed with a HFD.

ParameterControlHFDHFD + exercise
Body weight (g) 4.12±0.28 11.34±1.08a 9.58±1.66a
Visceral fat weight (g) 0.49±0.08 1.71±0.31a 1.08±0.11a,b
Total cholesterol (mg/dl) 99.34±8.32 148.23±6.77a 120.08±7.11a,b
Triglycerides (mg/dl) 70.11±5.28 97.13±6.25a 80.71±4.01a,b
High-density lipoprotein (mg/dl) 63.65±8.63 (4) 62.81±7.56 64.22±7.93

{ label (or @symbol) needed for fn[@id='tfn1-br-0-0-972'] } Values are presented as means ± standard error of the mean (n=7).

a P<0.05 vs. control

b P<0.05 vs. HFD group. HFD, high fat diet.

Exercise prevented HFD-induced impairment of vascular function

Aortic endothelium-dependent dilation responses to acetylcholine were decreased in the HFD mice compared with the control C57BL/6J mice fed with regular mouse chow, and these abnormalities were prevented in the HFD with swimming exercise group (Fig. 1A and Table II). However, no differences in sodium nitroprusside-induced aortic endothelium-independent dilation responses were observed between the three groups (Fig. 1B and Table II), indicating that exercise prevented HFD-induced impairment of the aortic endothelium-dependent relaxation function.

Table II.

Exercise improved aortic relaxation (%) in mice fed with a HFD.

Table II.

Exercise improved aortic relaxation (%) in mice fed with a HFD.

ControlHFDHFD + exercise

Dose (mol)AchSNPAchSNPAchSNP
1×10−9 0.78±0.53 0.45±0.35 5.93±5.16 3.52±1.97 2.49±1.26 0.42±0.21
3×10−9 3.29±1.76 6.72±4.91 7.13±2.18
1×10−8 9.36±3.33 3.39±1.74 10.73±4.87 9.36±3.68 11.72±2.59 7.48±1.69
3×10−8 20.67±5.03 12.61±4.63 15.99±3.40
1×10−7 36.51±4.22 46.92±6.91 20.27±7.41 38.39±5.38 34.83±3.95 33.31±5.03
3×10−7 41.16±5.71 32.61±6.46 34.14±4.92
1×10−6 50.45±5.45 66.06±8.64 44.18±6.30 65.91± 3.45 49.84±5.82 62.07±5.14
3×10−6 62.67±6.66 49.59±5.28 53.10±6.83
1×10−5 67.80±4.90 83.44±8.50 50.70±3.05a 79.67±3.64 60.17±4.06b 78.81±4.23
3×10−5 69.52±4.73 51.55±2.83a 65.84±3.55b
1×10−4 71.85±4.36 85.18±8.00 58.53±2.20a 83.21±3.72 66.10±4.49 80.28±4.36

{ label (or @symbol) needed for fn[@id='tfn4-br-0-0-972'] } Values are presented as means ± standard error (n=7).

a P<0.05 vs. CD

b P<0.05 vs. HFD group. HFD, high fat diet; Ach, acetylcholine; SNP, sodium nitroprusside.

Exercise prevented HFD-induced oxidative stress and proinflammatory adipokine expression

HFD induced increases in oxidant stress, assessed by ROS assay in the aortic tissues compared with the control C57BL/6J mice fed with regular mouse chow (Fig. 2A). In addition, HFD increased the proinflammatory adipokine expression of leptin and resistin, and inhibited the anti-inflammatory adipokine expression of adiponectin (Fig. 2B-D). However, swimming exercise significantly prevented these HFD-induced abnormalities (Fig. 2).

Exercise prevented HFD-induced proinflammatory response

The levels of the pro-inflammatory transcripts, MCP1, IL6 and IL8 were elevated in the aortic samples from HFD mice compared with those of the control mice fed with regular mouse chow (Fig. 3). However, swimming exercise significantly decreased the HFD-induced aortic proinflammatory response demonstrated by decreased expression levels of MCP1, IL6 and IL8 (Fig. 3).

Exercise inhibited HFD-induced angiogenesis in skeletal muscle

To reveal the effect of HFD on angiogenesis, the protein expression level of angiogenic factor, VEGF was measured. The protein expression level of VEGF was greater in the skeletal muscles of HFD mice compared with the control mice (Fig. 4). However, swimming exercise significantly decreased HFD-induced VEGF expression levels in the gastrocnemius skeletal muscle samples (Fig. 4).


The primary finding in the current study is that was that consumption of a HFD for 16 weeks induced increases in plasma dyslipidemia, oxidative stress, proinflammatory adipokines/cytokines, as well as skeletal muscle angiogenesis. These pathophysiological changes contributed to impairment of aortic endothelium-dependent dilation. Furthermore, swimming exercise prevented HFD-increased dyslipidemia, ROS, proinflammatory adipokines/cytokines, skeletal muscle VEGF expression and associated aortic dysfunction. The current findings are of considerable translational importance, as obesity and sedentary lifestyles are strongly associated with vascular dysfunction and CVD.

Dyslipidemia, one of the pathophysiological characteristics in obese patients, includes high levels of plasma TC and TG, low levels of HDL, and is key in the development of CVD in obese patients (12). For example, in a large series of 26,000 overweight children, 14.1% of patients had abnormal TC levels, 15.8% of patients had abnormal LDL-C, 11.1% of patients had abnormal HDL-C and 14.3% of patients had abnormal TG levels (13). Consistent with these data, the present study demonstrated that HFD induced increases in body weight and visceral fat body weight using abnormal lipid profile assays. The coexistence of these pathophysiological changes markedly aggravated the lipid accumulation and impaired aortic endothelium-dependent dilation in the present study. Thus, acetylcholine may induce aortic dilation via NO production and bioavailability, and sodium nitroprusside may induce vascular smooth muscle cell relaxation via NO/cyclic guanosine monophosphate/protein kinase G signaling pathways (14,15).

Increased oxidative stress is one of the underlying mechanisms in obesity-induced CVD (16). The Framingham study demonstrated that there was an increase in urinary levels of 8-epi-prostaglandin F2α, which is a systemic oxidative stress marker and was significantly linked to body mass index in 2,828 obese individuals (17). ROS are produced during mitochondrial respiration, as well as from outside the mitochondria, via free fatty acid β-oxidation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, xanthine oxidase, lipoxygenase and cyclooxygenases (18,19). As anticipated, HFD increased the level of aortic ROS, serum leptin and resistin, which further prompted aortic tissue maladaptive immune response and release of proinflammatory cytokines, including MCP1, IL6 and IL8. It has been demonstrated that HFD and high-fructose beverages increased body weight, leptin, inflammation and insulin resistance that are associated with steatosis, and oxidative stress in plasma and tissues, indicating that oxidative stress and inflammation are important contributors to the pathogenesis of CVD (20,21).

Recent studies have shown that physical activity decreases the risk of chronic diseases, and improves quality of life, as well as increasing life expectancy (22,23). For example, exercise increases atheroprotection by inhibition of oxidative stress and inflammation through two distinct signaling pathways (24). Exercise increases laminar shear stress activation to decrease ROS activity and to preserve endothelial NO bioavailability (25). Furthermore, exercise increases expression levels of anti-inflammatory cytokines in adipose tissue (25). One study indicated that exercise improves mitochondrial performance, and thus decreases ROS production and maladaptive immune response (26). Consistent with these studies, the present study further identified that exercise increased anti-inflammatory adipokine adiponectin expression levels and inhibited proinflammatory adipokine expression levels of leptin and resistin. Therefore, exercise or physical activity exerts protective effects in the pathologic conditions of over-nutrition and obesity, as well as other CVDs.

In the present study, HFD increased VEGF expression levels in skeletal muscle, which is an important marker for angiogenesis, indicating that HFD prompts mouse obesity and endothelial function impairment that further induce VEGF expression and angiogenesis with a feed-back mechanism. Other factors, such as VEGFs, PDGFs, angiopoietins and fibroblast growth factors are involved in regulating angiogenesis (27).

In conclusion, these data demonstrate that exercise prevented HFD-induced impairment of aortic dysfunction, and these protective effects were accompanied by a reduction in ROS and expression of inflammatory cytokines. The link between increased ROS, maladaptive immune responses, and aortic dysfunction offers the potential for identifying the origins of the impairment of vascular function and contributes to further development of novel therapeutic strategies.


The present study was supported by Xianning Science Funding (grant no. XN201516) to Dr Jun Fang.



Ramalho L, da Jornada MN, Antunes LC and Hidalgo MP: Metabolic disturbances due to a high-fat diet in a non-insulin-resistant animal model. Nutr Diabetes. 7:e2452017. View Article : Google Scholar : PubMed/NCBI


Huang S, Liu H, Meng N, Li B and Wang J: Hypolipidemic and Antioxidant effects of Malus toringoides (Rehd.) hughes leaves in high-fat-diet-induced hyperlipidemic rats. J Med Food. 20:258–264. 2017. View Article : Google Scholar : PubMed/NCBI


Lim S and Meigs JB: Links between ectopic fat and vascular disease in humans. Arterioscler Thromb Vasc Biol. 34:1820–1826. 2014. View Article : Google Scholar : PubMed/NCBI


Townsend RR: Arterial stiffness: Recommendations and Standardization. Pulse Basel. 4 Suppl 1:3–7. 2017. View Article : Google Scholar : PubMed/NCBI


Yamaguchi R, Yamamoto T, Sakamoto A, Ishimaru Y, Narahara S, Sugiuchi H and Yamaguchi Y: Chemokine profiles of human visceral adipocytes from cryopreserved preadipocytes: Neutrophil activation and induction of nuclear factor-kappa B repressing factor. Life Sci. 143:225–230. 2015. View Article : Google Scholar : PubMed/NCBI


Selcuk A, Bulucu F, Kalafat F, Cakar M, Demirbas S, Karaman M, Ay SA, Saglam K, Balta S, Demirkol S, et al: Skinfold thickness as a predictor of arterial stiffness: Obesity and fatness linked to higher stiffness measurements in hypertensive patients. Clin Exp Hypertens. 35:459–464. 2013. View Article : Google Scholar : PubMed/NCBI


Park SY, Rossman MJ, Gifford JR, Bharath LP, Bauersachs J, Richardson RS, Abel ED, Symons JD and Riehle C: Exercise training improves vascular mitochondrial function. Am J Physiol Heart Circ Physiol. 310:H821–H829. 2016.PubMed/NCBI


Morishima T, Restaino RM, Walsh LK, Kanaley JA, Fadel PJ and Padilla J: Prolonged sitting-induced leg endothelial dysfunction is prevented by fidgeting. Am J Physiol Heart Circ Physiol. 311:H177–H182. 2016. View Article : Google Scholar : PubMed/NCBI


Li YY, Shi ZM, Yu XY, Feng P and Wang XJ: Urotensin II-induced insulin resistance is mediated by NADPH oxidase-derived reactive oxygen species in HepG2 cells. World J Gastroenterol. 22:5769–5779. 2016. View Article : Google Scholar : PubMed/NCBI


Yan Q, Liu Q, Zweier JL and Liu X: Potency of authentic nitric oxide in inducing aortic relaxation. Pharmacol Res. 55:329–334. 2007. View Article : Google Scholar : PubMed/NCBI


Tang M and Fang J: TNF-α regulates apoptosis of human vascular smooth muscle cells through gap junctions. Mol Med Rep. 15:1407–1411. 2017. View Article : Google Scholar : PubMed/NCBI


Zhang FL, Xing YQ, Wu YH, Liu HY, Luo Y, Sun MS, Guo ZN and Yang Y: The prevalence, awareness, treatment, and control of dyslipidemia in northeast China: A population-based cross-sectional survey. Lipids Health Dis. 16:612017. View Article : Google Scholar : PubMed/NCBI


Raj M: Obesity and cardiovascular risk in children and adolescents. Indian J Endocrinol Metab. 16:13–19. 2012. View Article : Google Scholar : PubMed/NCBI


Yamashita T, Kawashima S, Ohashi Y, Ozaki M, Rikitake Y, Inoue N, Hirata K, Akita H and Yokoyama M: Mechanisms of reduced nitric oxide/cGMP-mediated vasorelaxation in transgenic mice overexpressing endothelial nitric oxide synthase. Hypertension. 36:97–102. 2000. View Article : Google Scholar : PubMed/NCBI


Rodriguez-Pascual F, Miras-Portugal MT and Torres M: Effect of cyclic GMP-increasing agents nitric oxide and C-type natriuretic peptide on bovine chromaffin cell function: Inhibitory role mediated by cyclic GMP-dependent protein kinase. Mol Pharmacol. 49:1058–1070. 1996.PubMed/NCBI


Rios FJ, Neves KB, Nguyen Dinh Cat A, Even S, Palacios R, Montezano AC and Touyz RM: Cholesteryl ester-transfer protein inhibitors stimulate aldosterone biosynthesis in adipocytes through Nox-dependent processes. J Pharmacol Exp Ther. 353:27–34. 2015. View Article : Google Scholar : PubMed/NCBI


Keaney JF Jr, Larson MG, Vasan RS, Wilson PW, Lipinska I, Corey D, Massaro JM, Sutherland P, Vita JA and Benjamin EJ: Framingham Study: Obesity and systemic oxidative stress: Clinical correlates of oxidative stress in the Framingham Study. Arterioscler Thromb Vasc Biol. 23:434–439. 2003. View Article : Google Scholar : PubMed/NCBI


Csányi G and Miller FJ Jr: Oxidative stress in cardiovascular disease. Int J Mol Sci. 15:6002–6008. 2014. View Article : Google Scholar : PubMed/NCBI


Rocha M, Apostolova N, Hernandez-Mijares A, Herance R and Victor VM: Oxidative stress and endothelial dysfunction in cardiovascular disease: Mitochondria-targeted therapeutics. Curr Med Chem. 17:3827–3841. 2010. View Article : Google Scholar : PubMed/NCBI


Lozano I, Van der Werf R, Bietiger W, Seyfritz E, Peronet C, Pinget M, Jeandidier N, Maillard E, Marchioni E, Sigrist S, et al: High-fructose and high-fat diet-induced disorders in rats: Impact on diabetes risk, hepatic and vascular complications. Nutr Metab (Lond). 13:152016. View Article : Google Scholar : PubMed/NCBI


Guo X, Li J, Tang R, Zhang G, Zeng H, Wood RJ and Liu Z: High fat diet alters gut microbiota and the expression of paneth cell-antimicrobial peptides preceding changes of circulating inflammatory cytokines. Mediators Inflamm. 2017:94748962017. View Article : Google Scholar : PubMed/NCBI


Wong A, Sanchez-Gonzalez M, Kalfon R, Alvarez-Alvarado S and Figueroa A: The effects of stretching training on cardiac autonomic function in obese postmenopausal women. Altern Ther Health Med. 23:20–26. 2017.PubMed/NCBI


Toyama K, Sugiyama S, Oka H, Hamada M, Iwasaki Y, Horio E, Rokutanda T, Nakamura S, Spin JM, Tsao PS, et al: A pilot study: The beneficial effects of combined statin-exercise therapy on cognitive function in patients with coronary artery disease and mild cognitive decline. Intern Med. 56:641–649. 2017. View Article : Google Scholar : PubMed/NCBI


Onat A: Metabolic syndrome: Nature, therapeutic solutions and options. Expert Opin Pharmacother. 12:1887–1900. 2011. View Article : Google Scholar : PubMed/NCBI


Szostak J and Laurant P: The forgotten face of regular physical exercise: A ‘natural’ anti-atherogenic activity. Clin Sci (Lond). 121:91–106. 2011. View Article : Google Scholar : PubMed/NCBI


Peeri M and Amiri S: Protective effects of exercise in metabolic disorders are mediated by inhibition of mitochondrial-derived sterile inflammation. Med Hypotheses. 85:707–709. 2015. View Article : Google Scholar : PubMed/NCBI


Silvennoinen M, Rinnankoski-Tuikka R, Vuento M, Hulmi JJ, Torvinen S, Lehti M, Kivelä R and Kainulainen H: High-fat feeding induces angiogenesis in skeletal muscle and activates angiogenic pathways in capillaries. Angiogenesis. 16:297–307. 2013. View Article : Google Scholar : PubMed/NCBI

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Fang J and Fang J: Exercise improves high fat diet-impaired vascular function. Biomed Rep 7: 337-342, 2017
Fang, J., & Fang, J. (2017). Exercise improves high fat diet-impaired vascular function. Biomedical Reports, 7, 337-342. https://doi.org/10.3892/br.2017.972
Fang, J., Tang, M."Exercise improves high fat diet-impaired vascular function". Biomedical Reports 7.4 (2017): 337-342.
Fang, J., Tang, M."Exercise improves high fat diet-impaired vascular function". Biomedical Reports 7, no. 4 (2017): 337-342. https://doi.org/10.3892/br.2017.972