Metabolic Syndrome-related Factors Research Articles

Low hair copper concentration is related to a high risk of nonalcoholic fatty liver disease in adults

Copper, an essential micronutrient, is required for lipid metabolism, mitochondrial function, iron metabolism, and antioxidant defense. Copper deficiency has been linked to alterations in lipid metabolism and various metabolic processes of the liver, including nonalcoholic fatty liver disease (NAFLD); however, most of these studies relied on copper measurements in the blood or tissues. In this study, we investigated the association between hair copper concentration and NAFLD in Korean adults, independent of metabolic syndrome status. Clinical and laboratory parameters, including factors of metabolic syndrome, were analyzed in 751 Korean adults divided into quintiles, according to hair copper concentration. Lower hair copper concentration was significantly correlated with higher body mass index, waist circumference, blood pressure, and lower levels of high-density lipoprotein cholesterol. Subjects with NAFLD showed significantly lower hair copper concentrations, and the risk of NAFLD was significantly higher for the lower hair copper quintile groups even after adjusting for metabolic syndrome-related factors. Overall, this study suggests that lower hair copper concentration could be associated with NAFLD, independent of metabolic syndrome factors.

Correlation between obesity and metabolic syndrome-related factors and cecal intubation time during colonoscopy.

PurposeTo investigate which colonoscopy (CS) cases should be presided over by endoscopists in training, using factors including obesity and metabolic syndrome.Patients and methodsItems investigated were sex, age, body mass index (BMI), waist circumference, hypertension, diabetes, hyperlipidemia, history of abdominal surgery (excluding colectomy), colon diverticulosis, prescription of antithrombotic agents, and quality of bowel preparation. Expert physicians were defined as those with at least 9 years of endoscopy experience; all other physicians were defined as being in training. In a retrospective analysis, cases in which a physician in training reached the cecum within 15 minutes without requiring the involvement of the supervising physician were defined as eligible cases over which a physician in training should preside, while other cases were defined as non-eligible.ResultsOverall, 813 CS cases were analyzed. Males (P<0.0001), cases started by an expert physician (P<0.0001), cases of no fellow physician involvement (P<0.0001), and cases with good bowel preparation (P<0.0001) had significantly shorter cecal intubation times. Of the 562 cases presided over by a physician in training, 194 were deemed eligible and 368 non-eligible. The eligible cases had a higher proportion of males (P=0.017), younger age (P=0.033), higher BMI (P=0.034), and higher rates of hypertension (P=0.001) and good bowel preparation (P=0.001). In analysis by sex, males demonstrated significantly more eligible cases among younger patients (P=0.009) and those with good bowel preparation (P=0.008), while there were significantly more eligible cases among females with hypertension (P=0.004).ConclusionIt may be useful to select CS cases for physicians considering sex, age, BMI, hypertension, and bowel preparation.

Additive Effects of Maternal High Fat Diet during Lactation on Mouse Offspring

Recent reports indicated that nutrition in early infancy might influence later child health outcomes such as obesity and metabolic syndrome. Therefore, we examined the effects of maternal high fat diet (HFD) during lactation on the onset of a metabolic syndrome in their offspring. All offspring were cross-fostered by dams on the same or opposite diet to yield 4 groups: offspring from HFD-fed dams suckled by HFD-fed dams (OHH) and by control diet (CD)-fed dams (OHC) and CD-fed dams suckled by HFD-fed dams (OCH) and by CD-fed dams (OCC) mice. We examined several metabolic syndrome-related factors including body weight, blood pressure, glucose tolerance and adipocytokines. Mean body weights of OHH and OCH mice were significantly higher than those of OHC and OCC mice, respectively, with elevated systolic blood pressure. Moreover, OHH and OCH mice revealed significantly worse glucose tolerance compared with the OHC and OCC mice, respectively. Triglyceride and leptin levels were significantly increased and adiponectin levels were significantly reduced by the maternal HFD during lactation, with similar changes in leptin and adiponectin mRNA expression but without histone modifications in adipose tissues. In addition, maternal obesity induced by HFD during lactation increased and prolonged the leptin surge in the offspring and the gender differences of leptin surge were observed. Our data suggested that maternal HFD during lactation might have an additive effect on the onset of the metabolic syndrome in the offspring, irrespective of the nutritional status in utero through the modified leptin surge.

걷기운동과 행동수정 프로그램이 비만 남중생의 체조성, 혈중지질 및 대사증후군 인자에 미치는 영향

The purpose of this study was to provide the obese middle school boys with walking and behavior modification program(WBMP) by investigating effects of the exercise on their body composition(BC), blood lipid(BL) and metabolic syndrome(MS). Analysis result of the difference between before and after the exercise(paired t-test and 2-way repeated ANOVA) was acquired by measuring BC, BL and MS for 12 weeks(60 min/day, three a week). 30 Volunteers were 14 years over ≥26.5kg/m2 and 15 years over ≥27.15 kg/m2. In the body composition, weight, %fat, body mass index(BMI), basic metabolic rate(BMR) were significant difference between the exercise group(EG) and the control group(CG), but height, lean body mass(LBM) were no difference. In the blood lipid, TC, LDL-C, insulin, leptin, IGF-I were significant difference between EG and CG, but growth hormone(GH) was no difference. In the metabolic syndrome related factors, waist circumference(WC), glucose, triglyceride, HDL-C, systolic and diastolic blood pressure were significant difference between EG and CG. The prevalence of metabolic syndrome was 11 of 30(36.7%) before intervention, but it dropped from 6 to 1 after intervention in WBMP. The components of metabolic syndrome was distributed a wide WC low HDL-C high TG hypertension high fasting blood glucose.

Dairy product consumption, calcium intakes, and metabolic syndrome–related factors over 5 years in the STANISLAS study

ObjectiveWe assessed the associations of total dairy products; milk, yogurt, and cottage cheese; cheese; and calcium with 5-y changes in components of the metabolic syndrome. MethodsTwo hundred eighty-eight men and 300 women 28 to 60 y of age from the suivi temporaire annuel non invasif de la santé des lorrains assurés sociaux (STANISLAS) cohort completed at baseline a 3-d dietary record. Statistics were performed using multivariate regression analysis. ResultsIn men, no relation was found between the four dietary indices and components of the metabolic syndrome measured at baseline. Conversely, the consumption of milk, yogurt, and cottage cheese at entry was inversely associated with 5-y changes in glucose levels (P ≤ 0.05, P ≤ 0.01 for sex interaction) and positively with 5-y changes in high-density lipoprotein cholesterol (P ≤ 0.05). Higher calcium intakes were significantly related to a lower 5-y increase of the body mass index (BMI) and waist circumference in men (P ≤ 0.01, P ≤ 0.05 for sex interaction). In addition, changes in diastolic blood pressure were inversely associated with the consumption of milk, yogurt, and cottage cheese only in men with a normal BMI (P ≤ 0.05 for BMI interaction). In women, unlike men, associations were shown for some components measured at baseline: total dairy positively related to BMI and waist circumference; total dairy, milk, yogurt, and cottage cheese, and calcium were positively related to triacylglycerols and negatively to high-density lipoprotein cholesterol. However, no significant association was found for any 5-y-changes. ConclusionIn men only, a higher consumption of dairy products was associated with positive changes in the metabolic profile in a 5-y period; a higher calcium consumption was associated with a lower 5-y increase of the BMI and waist circumference.

Role of High Molecular Weight Adiponectin in the Correlation Between Higher B-type Natriuretic Peptide Level and Accumulation of Metabolic Syndrome-Related Factors—Examination in Japanese Mass Screening

Role of High Molecular Weight Adiponectin in the Correlation Between Higher B-type Natriuretic Peptide Level and Accumulation of Metabolic Syndrome-Related Factors—Examination in Japanese Mass Screening

Effect of Keishibukuryogan on Endothelial Function in Patients with at Least One Component of the Diagnostic Criteria for Metabolic Syndrome: A Controlled Clinical Trial with Crossover Design

We evaluated the effect of keishibukuryogan (KBG; Guizhi-Fuling-Wan), a traditional Japanese (Kampo) formula, on endothelial function assessed by reactive hyperemia peripheral arterial tonometry (Endo-PAT2000) in patients with metabolic syndrome-related factors by controlled clinical trial with crossover design. Ninety-two patients were assigned to group A (first KBG-treatment period, then control period; each lasting 4 weeks, with about one-year interval) or group B (first control, then KBG-treatment). In forty-nine (27, group A; 22, group B) patients completing all tests, the mean value of the natural logarithmic-scaled reactive hyperemia index (L_RHI) increased and those of serum nonesterified fatty acid (NEFA), malondialdehyde, and soluble vascular cell adhesion molecule 1 decreased significantly during the KBG-treatment period, but not during the control period, and 4-week changes of L_RHI, NEFA, and malondialdehyde between the 2 periods showed significance. These results suggest that KBG has beneficial effect on endothelial function in patients with metabolic syndrome-related factors.

Simultaneous exposure of non-diabetics to high levels of dioxins and mercury increases their risk of insulin resistance

Insulin resistance and the defective function of pancreatic β-cells can occur several years before the development of type 2 diabetes. It is necessary to investigate and clarify the integrated effects of moderate-to-high exposure to dioxins and mercury on the pancreatic endocrine function. This cross-sectional study investigated 1449 non-diabetic residents near a deserted pentachlorophenol and chloralkali factory. Metabolic syndrome related factors were measured to examine associations with serum dioxin and blood mercury. We also investigated associations between insulin resistance (HOMA-IR > 75th percentile), defective pancreatic β-cells function (HOMA β-cell > 75th percentile), serum dioxins and blood mercury. After adjusting for confounding factors, we found that insulin resistance increased with serum dioxins ( b = 0.13, P < 0.001) and blood mercury ( b = 0.01, P < 0.001). Moreover, participants with higher serum dioxins or blood mercury were at a significantly increasing risk for insulin resistance ( P trend < 0.001). The joint highest tertile of serum dioxins and blood mercury was associated with elevated HOMA-IR at 11 times the odds of the joint lowest tertile (AOR 11.00, 95% CI: 4.87, 26.63). We hypothesize that simultaneous exposure to dioxins and mercury heightens the risk of insulin resistance more than does individual exposure.

Mineralocorticoid Receptors, Salt-Sensitive Hypertension, and Metabolic Syndrome

Obese persons with metabolic syndrome often have associated with salt-sensitive hypertension, microalbuminuria, and cardiac dysfunction, and the plasma aldosterone level in one-third of metabolic syndrome patients is clearly elevated. Hyperaldosteronism, which may be caused at least partially by certain adipocyte-derived factors, contributes to the development of proteinuria in obese hypertensive rats, and salt loading aggravates the proteinuria and induces cardiac diastolic dysfunction because of inadequate suppression of plasma aldosterone level. However, mineralocorticoid receptor (MR) antagonists prevent salt-induced renal and cardiac damage, suggesting that aldosterone excess and a high-salt diet exert an unfavorable synergistic action on the kidney and heart. In Dahl salt-sensitive rats, however, despite appropriate suppression of plasma aldosterone with a high-salt diet, salt loading paradoxically activated renal MR signaling, and the renal injury was markedly prevented by MR antagonists. Accordingly, we discovered an alternative pathway of MR activation in which Rac1, a small GTP-binding protein, activates MRs. Salt loading activates renal Rac1 in Dahl salt-sensitive rats, and Rac1 in turn induces MR activation, which results in renal injury, and the renal injury has been found to be prevented by Rac1 inhibitors. Moreover, several metabolic syndrome-related factors induce Rac1 activation, and one of them, hyperglycemia, activates MRs via Rac1 activation. Consistent with this, Rac1 inhibitors attenuated the proteinuria and renal injury in obese hypertensive animals. Thus, both salt and obesity activate Rac1 and cause MR activation. Abnormal activation of the aldosterone/MR pathway plays a key role in the development of salt-sensitive hypertension and renal injury in metabolic syndrome.

Ezetimibe Ameliorates Metabolic Disorders and Microalbuminuria in Patients with Hypercholesterolemia

Ezetimibe, an inhibitor of Niemann-Pick C1-like 1 protein, has been shown to reduce the intestinal absorption of cholesterol. We investigated whether it also has beneficial effects on metabolic disorder and/or renal insufficiency in patients with hypercholesterolemia. Ezetimibe was administered to 38 Japanese patients with hypercholesterolemia to obtain appropriate low-density lipoprotein cholesterol (LDL-chol) levels. Age- and sex-matched patients with hypercholesterolemia (n=38) were the controls. We evaluated the effects of ezetimibe before and 4 to 8 weeks after ezetimibe treatment. Ezetimibe significantly decreased LDL-chol levels and metabolic syndrome-related factors, including body weight, waist circumference, blood pressure; homeostasis model assessment insulin resistance (HOMA-IR), and urinary albumin excretion, were significantly reduced. In addition, it decreased the level of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-alpha, the urinary excretion of 8-hydroxy-2'-deoxyguanosine, a parameter of oxidative stress, and increased the urinary excretion of nitrate and nitrite (NOx). In the controls we observed no such changes. Excepting the decrease in the serum TNF-alpha level, the effects of ezetimibe were not correlated with decreased LDL-chol levels. Ezetimibe ameliorated the status of metabolic syndrome and microalbuminuria, reduced inflammation and oxidative stress, and increased nitric oxide bioavailability in a LDL-chol reduction-dependent and -independent manner.

Association Between Insulin Resistance and Co-Exposure to Dioxins and Mercury in Taiwanese Living Near a Deserted Pentachlorophenol and Chloralkali Factory

ISEE-0033 Background and Objective: Insulin resistance and the dysfunction of pancreatic b-cells can occur several years before the development of type 2 diabetes. Dioxins and mercury can cause pancreatic endocrine dysfunction in experimental animals. Because humans are exposed to dioxins and mercury primarily in fish that they eat, it is necessary to investigate and clarify the effects of the interaction of these two pollutants on the homoeostasis model assessment-insulin resistance (HOMA-IR) and pancreatic β-cell function. Methods: This cross-sectional study investigated 1449 non-diabetic residents near a deserted pentachlorophenol and chloralkali factory. Metabolic syndrome-related factors were measured to examine associations between serum dioxin and blood mercury levels. We also investigated associations between the risk of insulin resistance (HOMA-IR >75th percentile), pancreatic β-cell dysfunction (HOMA β-cell >75th percentile), serum dioxins, and blood mercury levels and their potential interaction. Results: After adjusting for confounding factors, residents with higher serum dioxin levels or blood mercury levels (reference: <25th percentile; higher: >75th percentile) were at a significant risk for insulin resistance (adjusted odds ratio [AOR] 4.0 [95% CI 2.3-7.3] for dioxins; AOR 2.3 [95% CI 1.5-3.5] for mercury) and HOMA β-cell dysfunction (AOR 2.5 [95% CI 1.4-4.3] only for dioxins). Residents with higher serum PCDD/F and blood mercury levels had a much greater risk of having insulin resistance (AOR 27.3 [95% CI 7.0-129.9]). In addition, participants with higher serum PCDD/F levels, but not for higher blood mercury levels, were at significant risk for having pancreatic β-cell dysfunction (AOR 2.3 [95% CI 1.3-3.9]) versus (AOR 1.0 [95% CI 0.7-1.6]), respectively. Conclusion: We found a significant association between serum PCDD/Fs, blood mercury, and insulin resistance after adjusting for confounding factors: interaction between dioxins, mercury, and insulin resistance exists even in persons without diabetes. Accumulated dioxins and mercury may synergistically increase the risk of developing insulin resistance.

The influence of metabolic syndrome components on plasma PAI-1 concentrations is modified by the PAI-1 4G/5G genotype and ethnicity

Coronary artery disease (CAD) is less common in African than Indian or White subjects and elevated plasminogen activator inhibitor (PAI)-1 levels may be a risk factor for CAD. Therefore, PAI-1 levels were measured in the three populations and related to the −675 PAI-1 4G/5G promoter genotype. PAI-1 levels and anthropometric variables were measured in 310 Indian, 269 White and 107 African subjects. The PAI-1 4G allele frequency was lower in the African (0.13) than Indian (0.54) or White (0.58) populations and explained the lower PAI-1 levels in African (41.5±25.1 versus 68.0±33.3 and 70.5±35.7ng/ml, respectively; p<0.0001) subjects. Except for White subjects, PAI-1 levels were higher in those with metabolic syndrome or type 2 diabetes. PAI-1 genotype did not associate with either disorder. Metabolic syndrome-related factors had little influence on PAI-1 levels in White subjects but in African and Indians subjects these variables had a major influence on PAI-1 levels in those with the 5G/5G genotype but not in subjects with the 4G/4G genotype. Ethnic differences in PAI-1 levels are largely due to differences in the frequency of the 4G and 5G alleles at the −675 locus. In Indian and African, but not White populations, the ability of metabolic syndrome-related factors to influence PAI-1 levels is modulated by the −675 genotype.