High-phosphorus/zinc-free diet aggravates hypertension and cardiac dysfunction in a rat model of the metabolic syndrome

BackgroundCardiac dysfunction is reported in patients with the metabolic syndrome. We assessed the effects of high-phosphorus and zinc-free diet on cardiovascular system in spontaneously hypertensive rats (SHR)/NDmcr-cp (SHR/cp), a rat model of the metabolic syndrome. We also investigated the effects of N-acetyl-L-cysteine (NAC), an antioxidant, on the development of cardiac dysfunction under such conditions.MethodsMale SHR/cp and control [Wistar Kyoto (WKY)] rats were divided into three groups and fed control diet (P 0.3% w/w, Zn 0.2% w/w) or high-phosphorus and zinc-free (P 1.2% w/w, Zn 0.0% w/w) diet. The latter group was treated with either NAC (1.5 mg/g per day) or vehicle from 6 to 18 weeks of age (n=6 or 8 for each group).ResultsHigh-phosphate and zinc-free diet increased systolic blood pressure in both WKY and SHR/cp. Echocardiography showed that high-phosphate and zinc-free diet markedly reduced left ventricular systolic and diastolic function in SHR/cp. Histopathologically, the same diet induced severe myocardial fibrosis in SHR/cp, and this effect was prevented by NAC. Whereas treatment with NAC prevented diastolic dysfunction induced by the same diet in WKY, it only improved systolic function but not diastolic function in SHR/cp.ConclusionsHigh-phosphate and zinc-free diet induced hypertension and cardiac dysfunction. These changes hamper the protective effects of NAC in the metabolic syndrome.SummaryThe present study showed that consumption of high-phosphorus and zinc-free diet increased the myocardial expression of connective tissue growth factor and reduced the expression of metallothionein, which enhanced the development of severe cardiac dysfunction in rats with the metabolic syndrome. The results suggest that the metabolic syndrome seems to aggravate cardiac dysfunction and hamper the protective effects of antioxidant, NAC.     

Rats with metabolic syndrome resist the protective effects of N-acetyl l-cystein against impaired spermatogenesis induced by high-phosphorus/zinc-free diet

Consumption of relatively high amounts of processed food can result in abnormal nutritional status, such as zinc deficiency or phosphorus excess. Moreover, hyperphosphatemia and hypozincemia are found in some patients with diabetic nephropathy and metabolic syndrome. The present study investigated the effects of high-phosphorus/zinc-free diet on the reproductive function of spontaneously hypertensive rats/NDmcr-cp (SHR/cp), a model of the metabolic syndrome. We also investigated the effects of antioxidant, N-acetyl-l-cysteine (NAC), on testicular dysfunction under such conditions. Male SHR/cp and control rats (Wistar Kyoto rats, WKY) were divided into three groups; rats fed control diet (P 0.3%, w/w; Zn 0.2%, w/w), high-phosphorus and zinc-deficient diet (P 1.2%, w/w; Zn 0.0%, w/w) with vehicle, or high-phosphorus and zinc-deficient diet with NAC (1.5 mg/g/day) for 12 weeks (n = 6 or 8 rats/group). The weights of testis and epididymis were significantly reduced by high-phosphate/zinc-free diet in both SHR/cp and WKY. The same diet significantly reduced caudal epididymal sperm count and motility and induced histopathological changes in the testis in both strains. Treatment with NAC provided significant protection against the toxic effects of the diet on testicular function in WKY, but not in SHR/cp. The lack of the protective effects of NAC on impaired spermatogenesis in SHR/cp could be due to the more pronounced state of oxidative stress observed in these rats compared with WKY.     

Diet modification and its influence on metabolic and related pathological alterations in the SHR/NDmcr-cp rat,an animal model of the metabolic syndrome

SHR/NDmcr-cp (SHR/NDcp) rats, which carry a nonsense mutation of the leptin receptor gene, are known to spontaneously develop hypertension, obesity and hyperlipidemia, and have therefore found use as an animal model of the metabolic syndrome and type 2 diabetes. However, some recent studies on SHR/NDcp rats revealed only mild elevation of blood glucose levels. To investigate whether metabolic factors including blood glucose and histopathological alterations of SHR/NDcp rats deteriorate with a diabetogenic diet, biochemical and histopathological examinations were conducted with animals fed normal or diabetogenic diets for 20 weeks. SHR/NDcp rats receiving the normal diet displayed obesity, hypertension, hyperlipidemia, and mild elevation of blood glucose and HbA1c levels. Urinary glucose excretion was noted in only 1 out of 6 animals. Histologically, macro- and micro-vesicular steatosis in the liver, glomerular and tubular damages in the kidney and islet hyperplasia mainly of beta cells in the pancreas were characteristically noted. In SHR/NDcp rats fed the diabetogenic diet, obesity was more severe, with higher blood glucose and HbA1c levels, increased numbers of animals with urinary glucose excretion, and more pronounced hepatic steatosis and renal tubular changes. However, elevation of blood glucose levels and urinary glucose excretion proved transient. These observations indicate that the diabetic state and associated histopathological alterations in SHR/NDcp rats are exacerbated by feeding a diabetogenic diet, but the effects are limited. Elevated islet function with compensative insulin secretion might be related to amelioration of the hyperglycemic state. Further diet modification could be needed to induce a more prominent and persistent diabetic state in SHR/NDcp rats.     

The importance of corticosterone in mediating restraint-induced weight loss in rats

I. J. Scherer, P. V. Holmes, R. B.S. Harris. The importance of corticosterone in mediating restraint-induced weight loss in rats. PHYSIOL BEHAV 00 (0) 000-000, 2010. Rats restrained for 3 h/day for 3 days (RR) lose weight and do not return to the weight of non-restrained controls once restraint has ended. This study tested the importance of restraint-induced corticosterone release in mediating the change in body weight by injecting ADX rats with 2.0 mg corticosterone/kg before each restraint to replicate the restraint-induced surge in circulating corticosterone. Restrained adrenalectomized (ADX) rats injected with corticosterone had the same initial weight loss as intact restrained rats, whereas corticosterone injection in non-restrained ADX rats and restraint of ADX rats injected with saline each produced only half as much initial weight loss. Sustained weight loss, measured for 14 days after the end of RR, was the same for restrained intact rats and restrained ADX rats injected with corticosterone whereas restrained ADX rats injected with saline achieved the same weight gain as their controls. Corticosterone injections had no effect on weight gain of non-restrained intact rats. In situ hybridization showed that corticotropin releasing factor (CRF) mRNA expression in the paraventricular nucleus of the hypothalamus (PVN) was increased by the same degree in ADX rats and restrained intact rats and was not modified by corticosterone injections. There was no significant effect of restraint, ADX or corticosterone injection on PVN arginine vasopressin (AVP) mRNA expression. These data indicate that a surge in corticosterone causes sustained weight loss in ADX rats through a mechanism that can be compensated for in intact rats and is independent of changes in PVN CRF or AVP mRNA expression.     

Metabolic syndrome and neurometabolic asymmetry of hippocampus in adult bonnet monkeys

Objective

Obesity is associated with the insulin resistance metabolic syndrome, postulated to be mediated by stress-induced alterations within the hypothalamic-pituitary-adrenal (HPA) axis. In adult bonnet macaques we examined relationships between components of the metabolic syndrome, hippocampal neurometabolic asymmetry, an indicator of negative affect, and juvenile cerebrospinal fluid (csf) corticotropin-releasing factor (CRF) levels obtained after stress exposure associated with maternal food insecurity and in controls.

Methods

Eleven adult male monkeys (seven with early life stress) who had undergone csf-CRF analyses as juveniles had magnetic resonance spectroscopic imaging (MRSI) of bilateral hippocampus, morphometry (body mass index, BMI; sagittal abdominal diameter, SAD) and determination of fasting plasma glucose and insulin as adults. Neurometabolite ratios included N-acetyl-aspartate as numerator (NAA; a marker of neuronal integrity) and choline (Cho; cell turnover) and creatine (Cr; reference analyte) as denominators.

Results

Elevated juvenile csf-CRF levels positively predicted adult BMI and SAD and were associated with right > left shift of NAA ratio within the hippocampus. Adult visceral obesity and insulin level correlated with right > left shift in hippocampal NAA concentrations, controlling for age and denominator.

Conclusion

Juvenile csf-CRF levels, a neuropeptide associated with early life stress, predict adult visceral obesity and hippocampal asymmetry supporting the hypothesis that metabolic syndrome in adults may be related to early life stress. Furthermore, this study demonstrates asymmetrical hippocampal alterations related to obesity.     

Menopause is an independent predictor of metabolic syndrome in Iranian women

Background

Gender differences in prevalence and consequences of the metabolic syndrome as a strong predictor of cardiovascular disease (CVD), are challenging problems. Postmenopausal status may explain in part the cause of acceleration of CVD with aging. The purpose of this study was to investigate the relation of menopause and metabolic syndrome independent of aging among Iranian women.

Methods

On the basis of consecutive recruitment, 940 women between 20 and 76 years old participated in the study. Anthropometric indices, fasting blood glucose, lipid profile were measured, Framingham risk score and homeostasis model assessment (HOMA-IR) were calculated for all participants. The metabolic syndrome (MetS) was defined according to the National Cholesterol Education Program Adult Treatment Panel III. We used IDF definition for metabolic syndrome modified by our recent local data as an alternative measurements.

Results

The overall prevalence of metabolic syndrome was 26.4%. Its prevalence was 53.5% in postmenopausal versus 18.3% in premenopausal women. On binary logistic regression analysis, HOMA index, body mass index, waist to hip ratio, family history of diabetes and hypertension had an independent and significant effect on metabolic syndrome. Age-adjusted odds ratio (OR) of postmenopausal status for metabolic syndrome was 2.85 (95%CI: 1.31–6.20) (P < 0.008). Framingham risk score was 8.3 ± 7.7 in MetS+ve cases versus 1.9 ± 2.1 in MetS−ve cases (P < 0.001). There were significant differences between Framingham risk score in postmenopause 9.1 ± 6.4 versus premenopause 1.6 ± 1.6 (P < 0.001). A significant correlation was found between Framingham risk score and body mass index, waist to hip ratio, HOMA-IR and components of metabolic syndrome (P < 0.001). Forty percent of participants with premature menopause had metabolic syndrome versus 24% in age-matched group and Framingham risk score was significantly higher than normal cases 5.4 ± 4.9 versus 2.0 ± 2.3 (P < 0.001).

Conclusion

Menopausal status can be a predictor of metabolic syndrome independent of age in Iranian women. Menopause is a process closely related to insulin resistance and cardiovascular risk factors.     

Myocardial disease and catecholamine metabolism in JCR:LA-corpulent rat

The JCR:LA-cp rat is a strain carrying the mutant cp (corpulent) gene. Animals that are homozygous cp are hyperphagous, hyperinsulinemic, hyperlipidemic, and obese. Corpulent male rats, but not females or lean rats, develop atherosclerotic lesions and myocardial lesions. Since the myocardial lesions are apparently of ischemic origin, the noradrenergic system and vascular hyperactivity and vasospasm may play a role in the pathogenesis. To test this we have studied the brain contents of the amines norepinephrine, dopamine, and 5-hydroxtryptamine and their breakdown products and depleted the peripheral sympathetic terminals with 6-hydroxydopamine. Only 5-hydroxytryptamine and 5 hydroxyindole-3-acetic acid were present at higher concentrations in the corpulent rats with depressed levels of dopamine in very young or old lean rats. The activity of monoamine oxidase may provide an indication of nonadrenergic activity in tissue. The activity in the heart increased with age and was higher in the corpulent rats than in the lean at all ages. Activity in aorta was independent of age or genotype. Long term treatment with 6-hydroxydopamine caused marked depletion of norepinephrine in the heart with only a slight decrease in brain concentration. There were no effects on the hyperlipidemia or hyperinsulinemia that are strongly associated with vascular and myocardial disease. The myocardial lesion frequency in corpulent rats was not altered by the chemical sympathectomy. The results suggest that norepinephrine and the sympathetic nervous system are probably not involved in the generation of the myocardial lesions or metabolic abnormalities in this strain of rat.     

The relationship between visfatin and metabolic syndrome in postmenopausal women

Objective

The biological role and activity of visfatin, an adipokine mainly produced by visceral fat, has not been fully elucidated. The observed relationships between visfatin and metabolisyndrome are inconsistent. The purpose of this study was to illuminate the relationship between visfatin and metabolic syndrome in postmenopausal women.

Methods

The present study included a sample of 110 postmenopausal Korean women. Subjects with cardiovascular disease or uncontrolled diabetes were excluded from the study sample. Body weight, height, blood pressure (BP), and waist and hip circumference were measured, and biochemical tests were performed.

Results

The mean serum visfatin level (mean ± SD) of subjects with metabolic syndrome was 2.74 ± 1.70 ng/ml. This was significantly higher than the mean level of subjects without metabolic syndrome (p < 0.01). As the number of components of metabolic syndrome increased, the concentration of serum visfatin also increased (p < 0.01). Visfatin concentration was positively correlated with age (r = 0.209, p < 0.05), waist circumference (r = 0.261, p < 0.01), systolic BP (r = 0.255, p < 0.01), diastolic BP (r = 0.252, p < 0.01), fasting glucose level (r = 0.278, p < 0.01), fasting insulin level (r = 0.313, p < 0.01), HOMA-IR (r = 0.345, p < 0.01), total cholesterol level (r = 0.213, p < 0.05), triglyceride level (r = 0.368, p < 0.01), WBC count (r = 0.352, p < 0.01), and homocysteine level (r = 0.196, p < 0.05). Using a multiple logistic regression analysis, visfatin was found to be an independent factor associated with metabolic syndrome after an adjustment for confounding variables including age, body mass index (BMI), and HOMA-IR.

Conclusions

Serum visfatin was associated with metabolic syndrome in postmenopausal women. This suggests that visfatin may act as the underlying pathophysiological trigger for metabolic syndrome in postmenopausal women.     

Hostility, metabolic syndrome, inflammation and cardiac control in young adults: The Young Finns Study

We studied whether there is an association between hostility and cardiovascular heart disease (CHD) risk factors, such as the metabolic syndrome, systemic inflammation and autonomic cardiac control. Participants were 912 women and 712 men aged 15-30 when hostility was measured in 1992. Metabolic syndrome was assessed 9 years later in 2001 using 3 definitions: the National Institute of Health Adult Treatment Panel III criteria (NCEP), the European Group for the Study of Insulin Resistance criteria (EGIR), and the International Diabetes Federation criteria (IDF). C-reactive protein (CRP) defined in 2001 was the marker of inflammation. Cardiac control indices were from EGC recording. In women, hostility predicted increased risk of metabolic syndrome (EGIR, and the IDF definitions, ORs = 1.34, 1.35, p < 0.05), and higher levels of inflammation (β = 0.09, p < 0.01). We concluded that hostility is associated with metabolic syndrome and systemic inflammation in women and these conditions may be factors linking hostility to CHD.     

Nonshivering thermogenesis in the diabetic SHR/N-cp (corpulent) rat

The effects of isoenergetic sucrose and starch-based diets on thermogenesis were investigated in young adult, male, lean and corpulent SHR/N-cp rats. Corpulent rats gained weight 1.5 times more rapidly than lean, and sucrose diets resulted in more rapid weight gains in both phenotypes. Rates of resting and of norepinephrine-stimulated oxygen consumption were similar in both groups of lean rats and in sucrose-fed corpulent rats, but were decreased in starch-fed corpulent rats. The thermic response to injected norepinephrine occurred normally in all groups. Colonic and rectal temperatures were greater in lean than in corpulent rats. Acute cold exposure (5 degrees C) resulted in decreases in rectal but not colonic temperature in lean rats fed both diets, but resulted in lower temperatures at both sites in corpulent rats, with the greatest decreases being observed in the starch fed corpulent rats. Fifty percent of the corpulent but none of the lean rats succumbed within 24-48 hours following cold exposure. Urinary vanilmandelic acid (VMA) excretion was greater in lean than in corpulent rats, and the sucrose diet induced a greater increment in urinary VMA excretion in lean rats than in corpulent rats. These results are consistent with an impaired activation of sympathetically-mediated thermogenesis via nutritional or environmental stimuli in the corpulent genotype of the SHR/N-cp rat in concert with an economy in energy expenditure which may be contributing factors in the causation of their obese state.     

Upregulation of GAD65 mRNA in the medulla of the rat model of metabolic syndrome

Metabolic syndrome is characterized by obesity, elevated blood pressure (BP), insulin resistance, and hypercholesterolemia. Recently an animal model of this disorder has been proposed in rats selectively bred based on their performance on a treadmill-running task. Accordingly, low capacity runner (LCR) rats exhibited all of the diagnostic criteria for metabolic syndrome, including elevated BP, as compared to their high capacity runner (HCR) counterparts [U. Wisløff, S.M. Najjar, O. Ellingsen, P.M. Haram, S. Swoap, Q. Al-Share, M. Fernstrom, K. Rezaei, S.J. Lee, L.G. Koch, S.L. Britton, Cardiovascular risk factors emerge after artificial selection for low aerobic capacity, Science 307 (2005) 418–420]. Previous studies have highlighted the importance of GABAergic neurotransmission in the medullary cardiovascular-regulatory areas in the central control of BP. Thus, we hypothesized a dysregulation in GABAergic transmission in the medullary cardiovascular-regulatory nuclei of LCR rats. To begin testing this hypothesis we carried out experiments examining expression of the GABA synthetic enzymes, GAD65 and GAD67, mRNAs in the two rat strains via radioactive in situ hybridization. Our results showed GAD65 and GAD67 mRNAs were widely expressed throughout the brainstem; quantification revealed increased GAD65 mRNA expression in LCR animals in the caudal nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (VLM) as compared to HCR rats. Conversely, no differences in the expression of GAD67 were detected in these regions. These data are consistent with the notion of altered GABAergic neurotransmission in the NTS and VLM in metabolic syndrome, and point to the importance of these regions in cardiovascular regulation.     

Long-term caloric restriction reduces metabolic rate and heart rate under cool and thermoneutral conditions in FBNF1 rats

The long-term metabolic and cardiovascular responses to caloric restriction (CR) are poorly understood. We examined the responses to one year of CR in FBNF1 rats housed in cool (COOL; T_a = 15 °C) or thermoneutral (TMN; T_a = 30 °C) conditions. Rats were acclimated to COOL or TMN for 2 months, instrumented for cardiovascular telemetry and studied in calorimeters. Baseline caloric intake, oxygen consumption (VO₂), mean arterial blood pressure (MAP), and heart rate (HR) were determined prior to assignment to ad lib (AL) or CR groups (30-40% CR) within each T_a (n = 8). Groups of rats were studied after 10 weeks CR, one year CR, and after 4 days of re-feeding. Both 10 weeks and one year of CR reduced HR and VO₂ irrespective of T_a. Evaluation of the relationship between metabolic organ mass (liver, heart, brain, and kidney mass) and energy expenditure revealed a clear shift induced by CR to reduce expenditure per unit metabolic mass in both COOL and TMN groups. Re-feeding resulted in prompt elevations of HR and VO₂ to levels observed in control rats. These findings are consistent with the hypothesis that long term CR produces sustained reductions in metabolic rate and heart rate in rats.     

Long-term normalization of blood pressure in SHR and 1-kidney 1-clip rats by synthetic precursor of stable PAF analogue without systemic effects in normotensive rats

This study characterized the actions of the newly synthesized PAF precursor 1-hexadecyl-2-alkylcarbamoyl-glycerol (HAG) on blood pressure (BP) in male spontaneously hypertensive rats (SHR), SHR-stroke prone (SHRSP) and Wistar rats with 1-kidney 1-clip (1K1C) renovascular hypertension used as experimental models of human primary and secondary hypertension. Systolic blood pressure (SBP) in the tail artery and mean arterial pressure (MAP) in the abdominal aorta were measured by tail plethysmography and invasive pressure transducer, respectively. Intravenous treatment with 1 mg/kg HAG in SHR resulted in a rapid decline of MAP from 151 ± 4 to 127 ± 4 mm Hg in 50 min (p < 0.001) that was maintained for 24 h after injection (128 ± 5 mm Hg, p < 0.01). We also observed a profound hypotensive effect of HAG in SHRSP but not in normotensive Wistar rats. In 1K1C rats, the magnitude of the BP decline evoked by HAG was correlated with MAP measured before drug administration (R = 0.74, p < 0.005). In 1K1C rats with SBP > 140 mm Hg, 5 mg/kg/48 h HAG, given orally for 14 days, decreased SBP by 20-30 mm Hg without an increase in the death rate and other adverse effects. Thus, our results show that intravenous and oral administration of HAG led to a long-lasting reduction of BP in experimental models of primary and secondary hypertension. In contrast to PAF and its derivatives, the hypotensive action of HAG was preserved for 24 h after a single administration, was absent in normotensive animals, and was not accompanied by visible side-effects, at least during 2 weeks of treatment.     

Transplantation or removal of intra-abdominal adipose tissue prevents age-induced glucose insensitivity

Increases in intra-abdominal fat, a common feature associated with aging, is an established risk factor for insulin resistance, diabetes and the metabolic syndrome. To examine the direct contribution of intra-abdominal fat in the pathophysiology of insulin resistance we altered fat volume via removal or transplantation in a naturally occurring age-induced moderate model of obesity and insulin resistance. This was accomplished by bilateral removal of epididymal white adipose tissue (Lipx) or transplantation of donor fat into the intra-abdominal side of the peritoneal cavity of 28-week old rats. Control animals received sham surgery. Glucose tolerance was evaluated at baseline and 4 and 8 weeks post-surgery in all groups, and fasting insulin and leptin were additionally measured in 28-week old rats. In addition, fasted and fed triglyceride, cholesterol and fatty acid concentrations were measured. Before surgery 28-week old rats weighed more and were glucose intolerant compared with 8-week old controls. Both Lipx and transplantation significantly prevented age-induced decreases in glucose tolerance, with Lipx causing improvement at 4 weeks which declined by 8 weeks; and with a significant transplantation improvement at 8 weeks only. Lipx significantly increased insulin secretion 15 min after a bolus injection of 0.75 mg/kg dextrose at 4 and 8 weeks compared with controls, while transplantation caused a significant (∼ 220%) increase in fasted leptin level at 4 weeks only. Taken together, these data suggest that surgical removal or addition of intra-abdominal fat prevents age-induced insulin resistance by different mechanisms and is a suitable model to investigate naturally occurring obesity.     

Intracerebroventricular administration of conjugated linoleic acid (CLA) inhibits food intake by decreasing gene expression of NPY and AgRP

Dietary conjugated linoleic acid (CLA) has been investigated for its beneficial effects on disease prevention and treatment, and now obesity is one of the most perspective researching highlights. In a variety of experimental models, the results of studies on the effects of CLA on food intakes are somewhat inconsistent. Our experiment was conducted to extend these observations to hypothalamus and other regions within the central nervous system so that the mechanism of the actions of CLA might be more easily elucidated. In the experiment, a permanent cannula was inserted into the lateral ventricle of each rat. For the experiment, animals received intracerebroventricular injections of either 150 nmol (n = 16) CLA, or LA as non-conjugated control, or normal saline as vehicle. Hypothalamus and blood samples were collected at the 2nd, 4th, 8th, and 14th day. The results show that CLA in cerebral ventricle can inhibit food intake of experimented rats and this inhibition is related with the decreased expression of neuropeptides Y (NPY) and agouti-related protein (AgRP). The circulating leptin level was also increased by this tentative treatment (2.94 ± 0.71 versus 1.18 ± 0.18 ng/ml). However, the glucose metabolism was not affected by ICV CLA. It is concluded that CLA in brain can inhibit the appetite of rats through the mechanism of decreasing the expression of NPY and AgRP.     

The effect of different bovine viral diarrhea virus genotypes and biotypes on the metabolic activity and activation status of bovine peripheral blood mononuclear cells

The effects of cytopathic (cp) and non-cytopathic (ncp) bovine viral diarrhea virus (BVDV) on the cellular metabolic activity and activation status of bovine peripheral blood mononuclear cells (PBMC) were investigated. Cellular DNA and protein synthesis was determined by [3H]thymidine and [3H]valine incorporation, respectively, in phytohemagglutinin (PHA)-stimulated PBMC. All cp strains and most ncp BVDV strains significantly inhibited DNA synthesis in PHA-stimulated PBMC; however, only cp BVDV strains inhibited protein synthesis. A plaque assay and immunofluorescence test confirmed productive BVDV infection of PBMC. In addition, viral RNA synthesis was demonstrated in BVDV-infected PBMC by RT-PCR. The interleukin-2 receptor (IL-2R) was used as a marker for the activation status of BVDV-infected PBMC. The expression of IL-2R was preserved in virus-infected cells, even though DNA and protein synthesis was suppressed. These findings suggest a novel mechanism of virus-induced immune suppression in which BVDV inhibits basic metabolic activities of bovine PBMC. The activation signals, however, are maintained.     

Aerobic exercise training induces metabolic benefits in rats with metabolic syndrome independent of dietary changes

OBJECTIVES:

We evaluated the effects of aerobic exercise training without dietary changes on cardiovascular and metabolic variables and on the expression of glucose transporter Type 4 in rats with metabolic syndrome.

METHODS:

Twenty male spontaneously hypertensive rats received monosodium glutamate during the neonatal period. The animals were allocated to the following groups: MS (sedentary metabolic syndrome), MS-T (trained on a treadmill for 1 hour/day, 5 days/week for 10 weeks), H (sedentary spontaneously hypertensive rats) and H-T (trained spontaneously hypertensive rats). The Lee index, blood pressure (tail-cuff system), insulin sensitivity (insulin tolerance test) and functional capacity were evaluated before and after 10 weeks of training. Glucose transporter Type 4 expression was analyzed using Western blotting. The data were compared using analysis of variance (ANOVA) (p<0.05).

RESULTS:

At baseline, the MS rats exhibited lower insulin sensitivity and increased Lee index compared with the H rats. Training decreased the body weight and Lee index of the MS rats (MS-T vs. MS), but not of the H rats (H-T vs. H). There were no differences in food intake between the groups. At the end of the experiments, the systolic blood pressure was lower in the two trained groups than in their sedentary controls. Whole-body insulin sensitivity increased in the trained groups. Glucose transporter Type 4 content increased in the heart, white adipose tissue and gastrocnemius muscle of the trained groups relative to their respective untrained groups.

CONCLUSION:

In conclusion, the present study shows that an isolated aerobic exercise training intervention is an efficient means of improving several components of metabolic syndrome, that is, training reduces obesity and hypertension and increases insulin sensitivity.     

Depressive symptoms and sub-clinical atherosclerosis in Africans: role of metabolic syndrome, inflammation and sympathoadrenal function

Depressive symptoms have been consistently associated with sub-clinical atherosclerosis and future risk of coronary heart disease events. However, the pathways linking depression and coronary atherosclerosis are poorly understood. These types of data are particularly sparse in sub-Saharan Africa, which is presently experiencing an exponential rise in CVD. We examined the association between depressive symptoms and mean carotid intima media thickness (mCIMT), and the extent to which this association could be explained by sympathoadrenal function, inflammatory, and metabolic pathways. A sample of 186 black (aged 44.0 ± 8.0 years) and 203 Caucasians (aged 44.8 ± 10.8 years) were recruited as part of the Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study — presently the only study in sub-Saharan Africa focusing on the contribution of the psychosocial risk factors to cardiovascular health. Depressive symptoms were assessed using the self administered 9-item Patient Health Questionnaire. After adjusting for age, sex, ethnicity, and anti-hypertensive drugs use, participants with severe depressive symptoms had higher mCIMT in comparison to participants with no symptoms (β = 0.038 mm, 95% CI, 0.001 to 0.074 mm). Metabolic syndrome was the only significant mediator of the association between depressive symptoms and mCIMT, and accounted for approximately 21% of the effect. In summary, depressive symptoms were associated with an excess burden of sub-clinical vascular disease. Treatment of metabolic syndrome in patients with depression may partly reduce the risk of sub-clinical vascular disease development.     

Prevalence of parameter indicators of obesity and its relationship with metabolic syndrome in urban Moroccan women

This study aimed to examine the relationship between metabolic syndrome (MS) and different types of obesity in urban Moroccan women. On 213 women aged 25–55 years, Triglycerides (TG), total cholesterol, high‐density lipoprotein cholesterol (HDL‐c), lower‐density lipoprotein cholesterol (LDL‐c), and fasting blood glucose levels were assessed. Body mass index (BMI), waist to hip ratio (WHR), Waist circumference (WC), and blood pressure (BP) were also measured. Globally 36.6% of women were overweight (25 ≤ BMI < 30 m²), 23.9% obese (BMI > 30 m²), 19.7% had WHR > 0.85 and 28.8% had WC ≥ 88 cm. Indicators of obesity increased with age and the prevalence of co‐morbid factors increased with obesity. The women with android obesity (WHR > 0.85) and central obesity (WC ≥ 88 cm) had greater risk compared to those with overweight and general obesity. The prevalence of MS was 17.8% and increased (31.49%) with high BMI and high WHR (50%). MS and its co‐morbidity factors are prevalent among Moroccan women aged 35years and over. The exaggerated influence of obesity in this prevalence suggests that the prevention of obesity could prevent MS and its complications. Am. J. Hum. Biol., 2008. © 2008 Wiley‐Liss, Inc.