Black Beans, Fiber, and Antioxidant Capacity Pilot Study: Examination of Whole Foods vs. Functional Components on Postprandial Metabolic, Oxidative Stress, and Inflammation in Adults with Metabolic Syndrome.

Beans (Phaseolus vulgaris) contain bioactive components with functional properties that may modify cardiovascular risk. The aims of this pilot study were to evaluate the ability of black beans to attenuate postprandial metabolic, oxidative stress, and inflammatory responses and determine relative contribution of dietary fiber and antioxidant capacity of beans to the overall effect. In this randomized, controlled, crossover trial, 12 adults with metabolic syndrome (MetS) consumed one of three meals (black bean (BB), fiber matched (FM), and antioxidant capacity matched (AM)) on three occasions that included blood collection before (fasting) and five hours postprandially. Insulin was lower after the BB meal, compared to the FM or AM meals (p < 0.0001). A significant meal × time interaction was observed for plasma antioxidant capacity (p = 0.002) revealing differences over time: AM > BB > FM. Oxidized LDL (oxLDL) was not different by meal, although a trend for declining oxLDL was observed after the BB and AM meals at five hours compared to the FM meal. Triglycerides and interleukin-6 (IL-6) increased in response to meals (p < 0.0001). Inclusion of black beans with a typical Western-style meal attenuates postprandial insulin and moderately enhances postprandial antioxidant endpoints in adults with MetS, which could only be partly explained by fiber content and properties of antioxidant capacity

Blood pressure and cardiac autonomic nervous system in obese type 2 diabetic patients: Effect of metformin administration

Background: Hyperinsulinemia/insulin resistance and elevated plasma free fatty acids (FFA) levels are involved in the hypertension and cardiac sympathetic overactivity. Metformin improves insulin action and lower plasma FFA concentrations. We investigate the possible effect of metformin on arterial blood pressure (BP) and cardiac sympathetic nervous system. Methods: One hundred twenty overweight type 2 diabetic patients were treated by placebo (n = 60) + diet or metformin (850 mg twice daily) (n = 60) + diet for 4 months, to evaluate the effect of metformin treatment on the cardiac autonomic nervous system. Insulin resistance was measured by the Homeostasis Model Assessment (HOMA) index. Heart rate variability (HRV) assessed cardiac sympathovagal balance. Results: Metformin treatment, but not placebo treatment, was associated with a decrease in fasting plasma glucose (P < .05), insulin (P < .05), triglyceride (P < .05), and FFA (P < .03) concentrations and HOMA index (P < .03). Metformin treatment was also associated with a significant improvement in cardiac sympathovagal balance but not in mean arterial BP. Furthermore, in a multivariate analysis, delta change in sympathovagal balance index (LF/HF ratio) were associated with delta change in plasma FFA concentrations and HOMA index independently of gender and delta change in plasma triglyceride and HbA1c concentrations. Conclusions: Our study demonstrated that metformin treatment might be useful for improving cardiac sympathovagal balance in obese type 2 diabetic patients

SGLT2-inhibitors effects on the coronary fibrous cap thickness and MACEs in diabetic patients with inducible myocardial ischemia and multi vessels non-obstructive coronary artery stenosis

Background: Sodium-glucose transporter 2 inhibitors (SGLT2-I) could modulate atherosclerotic plaque progression, via down-regulation of inflammatory burden, and lead to reduction of major adverse cardiovascular events (MACEs) in type 2 diabetes mellitus (T2DM) patients with ischemic heart disease (IHD). T2DM patients with multivessel non-obstructive coronary stenosis (Mv-NOCS) have over-inflammation and over-lipids' plaque accumulation. This could reduce fibrous cap thickness (FCT), favoring plaque rupture and MACEs. Despite this, there is not conclusive data about the effects of SGLT2-I on atherosclerotic plaque phenotype and MACEs in Mv-NOCS patients with T2DM. Thus, in the current study, we evaluated SGLT2-I effects on Mv-NOCS patients with T2DM in terms of FCT increase, reduction of systemic and coronary plaque inflammation, and MACEs at 1&nbsp;year of follow-up. Methods: In a multi-center study, we evaluated 369 T2DM patients with Mv-NOCS divided in 258 (69.9%) patients that did not receive the SGLT2-I therapy (Non-SGLT2-I users), and 111 (30.1%) patients that were treated with SGLT2-I therapy (SGLT2-I users) after percutaneous coronary intervention (PCI) and optical coherence tomography (OCT) evaluation. As the primary study endpoint, we evaluated the effects of SGLT2-I on FCT changes at 1&nbsp;year of follow-up. As secondary endpoints, we evaluated at baseline and at 12&nbsp;months follow-up the inflammatory systemic and plaque burden and rate of MACEs, and predictors of MACE through multivariable analysis. Results: At 6 and 12&nbsp;months of follow-up, SGLT2-I users vs. Non-SGLT2-I users showed lower body mass index (BMI), glycemia, glycated hemoglobin, B-type natriuretic peptide, and inflammatory cells/molecules values (p &lt; 0.05). SGLT2-I users vs. Non-SGLT2-I users, as evaluated by OCT, evidenced the highest values of minimum FCT, and lowest values of lipid arc degree and macrophage grade (p &lt; 0.05). At the follow-up end, SGLT2-I users vs. Non-SGLT2-I users had a lower rate of MACEs [n 12 (10.8%) vs. n 57 (22.1%); p &lt; 0.05]. Finally, Hb1Ac values (1.930, [CI 95%: 1.149-2.176]), macrophage grade (1.188, [CI 95%: 1.073-1.315]), and SGLT2-I therapy (0.342, [CI 95%: 0.180-0.651]) were independent predictors of MACEs at 1&nbsp;year of follow-up. Conclusions: SGLT2-I therapy may reduce about 65% the risk to have MACEs at 1&nbsp;year of follow-up, via ameliorative effects on glucose homeostasis, and by the reduction of systemic inflammatory burden, and local effects on the atherosclerotic plaque inflammation, lipids' deposit, and FCT in Mv-NOCS patients with T2DM

Lipids in association with serum magnesium in diabetes mellitus patients

Background. The aim of the study was to investigate if and how, in diabetes mellitus (DM) patients, serum Magnesium (Mg) concentration influences serum lipids. A cross-sectional study was conducted on diabetic mellitus (DM) patients with various kidney functions, not yet on dialysis. Material and methods. Serum lipoprotein (a), glycosylated haemoglobin (HbA1c), serum magnesium (Mg), serum creatinine (creat) and serum lipids, consisting of triglycerides (Tg), cholesterol (Chol) and high density lipoprotein (HDL) were measured. Results. Study patients included 122 patients (82 F, 40 M). The mean patient's age was 63 (&plusmn; 10) years. The mean length of time they were diabetic was 7.4 (&plusmn; 5.8) years (median: 6 years). The mean serum Mg was 2 (&plusmn; 0.4) mg/dl (median: 1.99 mg/dl). The mean creatinine clearance was 64 (&plusmn; 24) cc/min (median: 64 cc/min). In this study significant inverse correlations of serum Mg with serum cholesterol and LDL, and also non significant correlations of serum Mg with serum Lp (a), HDL, Tg and with serum HbA1c were seen. Moreover, a significant inverse correlation of serum Mg with the patients' ages and a significant positive correlation of serum Mg with serum creatinine were also seen. Conclusions. It seems that in diabetic patients, kidney function is a key role in the regulation of serum Lp(a) levels instead of other factors like serum Mg level. Our findings further support the importance of Mg supplementation in diabetes mellitus patients. In our study no significant correlation between serum Mg with serum HDL and Tg were found, which needs further investigation.Background. The aim of the study was to investigate if and how, in diabetes mellitus (DM) patients, serum Magnesium (Mg) concentration influences serum lipids. A cross-sectional study was conducted on diabetic mellitus (DM) patients with various kidney functions, not yet on dialysis. Material and methods. Serum lipoprotein (a), glycosylated haemoglobin (HbA1c), serum magnesium (Mg), serum creatinine (creat) and serum lipids, consisting of triglycerides (Tg), cholesterol (Chol) and high density lipoprotein (HDL) were measured. Results. Study patients included 122 patients (82 F, 40 M). The mean patient's age was 63 (&plusmn; 10) years. The mean length of time they were diabetic was 7.4 (&plusmn; 5.8) years (median: 6 years). The mean serum Mg was 2 (&plusmn; 0.4) mg/dl (median: 1.99 mg/dl). The mean creatinine clearance was 64 (&plusmn; 24) cc/min (median: 64 cc/min). In this study significant inverse correlations of serum Mg with serum cholesterol and LDL, and also non significant correlations of serum Mg with serum Lp (a), HDL, Tg and with serum HbA1c were seen. Moreover, a significant inverse correlation of serum Mg with the patients' ages and a significant positive correlation of serum Mg with serum creatinine were also seen. Conclusions. It seems that in diabetic patients, kidney function is a key role in the regulation of serum Lp(a) levels instead of other factors like serum Mg level. Our findings further support the importance of Mg supplementation in diabetes mellitus patients. In our study no significant correlation between serum Mg with serum HDL and Tg were found, which needs further investigation

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

Serum Magnesium Concentrations and All-cause, Cardiovascular, and Cancer Mortality among U.S. Adults: Results from The NHANES I Epidemiologic Follow-up Study

Background Few studies have examined the associations of serum magnesium (Mg) concentrations with total and cause-specific mortality in a nationally representative sample of US adults. We investigate the dose–response relationships of baseline serum Mg concentrations with risk of mortalities in a large, nationally representative sample of US adults. Methods We analyzed prospective data of 14,353 participants aged 25–74 years with measures of serum Mg concentrations at baseline (1971–1975) from the National Health and Nutrition Examination Survey I Epidemiologic Follow-up Study (NHEFS). Mortality data was linked through December 31, 2011. We estimated the mortality hazard ratios (HRs), for participants within serum Mg categories of <0.7, 0.7–0.74, 0.75–0.79, 0.8–0.89 (referent), 0.9–0.94, 0.95–0.99, and ≥1.0 mmol/L using weighted multivariate-adjusted Cox proportional hazards models. Results During a median follow-up of 28.6 years, 9012 deaths occurred, including 3959 CVD deaths, 1923 cancer deaths, and 708 stroke deaths. The multivariate-adjusted HRs (95% CIs) of all-cause mortality across increasing categories of Mg were 1.34 (1.02, 1.77), 0.94 (0.75, 1.18), 1.08 (0.97, 1.19), 1.00 (referent), 1.05 (0.95, 1.16), 0.96 (0.79, 1.15), and 0.98 (0.76, 1.26). Similar trends were observed for cancer (HRs for serum Mg < 0.7: 1.39, 95% CI: 0.83, 2.32) and CVD mortality (HRs for serum Mg < 0.7: 1.28, 95% CI: 0.81, 2.02) but were not statistically significant. An elevated risk for stroke mortality was observed among participants with serum Mg < 0.70 mmol/L (HR: 2.55, 95% CI: 1.18, 5.48). Conclusions Very low serum Mg concentrations were significantly associated with an increased risk of all-cause mortality in US adults

The association between Metabolic Syndrome and serum levels of lipid peroxidation and interleukin-6 in Gorgan

Background: There are limited studies on the relationship between inflammatory marker such as IL-6 and lipid peroxidation and metabolic syndrome. Objective: The aim of present study was to assess IL-6 and lipid peroxidation in subjects with and without the metabolic syndrome and their association with metabolic syndrome components. Methods: Age and gender matched 40 subjects with metabolic syndrome and 40 control groups took part in this study. Results: The mean malondialdehyde level was significantly higher in overweight and obese subjects with metabolic syndrome than control groups (P. <. 0.05). The mean level of IL-6 in men and the mean level of malondialdehyde in women with metabolic syndrome was significantly higher than control groups (p <. 0.05). There were significant positive correlation between malondialdehyde and fasting blood glucose, triglyceride and systolic blood pressure (p <. 0.05). Conclusions: Our results suggest that higher levels of IL-6 and malondialdehyde may cause insulin resistance and metabolic disorders in all subjects with metabolic syndrome. Malondialdehyde level shows strong association with some metabolic syndrome components. This means the greater risk of metabolic syndrome. © 2015

Seven-year mortality in heart failure patients with undiagnosed diabetes : an observational study

Background: Patients with type 2 diabetes mellitus and heart failure have adverse clinical outcomes, but the characteristics and prognosis of those with undiagnosed diabetes in this setting has not been established. Methods: In total, 400 patients admitted consecutively with acute heart failure were grouped in three glycaemic categories: no diabetes, clinical diabetes (previously reported or with hypoglycaemic treatment) and undiagnosed diabetes. The latter was defined by the presence of at least two measurements of fasting plasma glycaemia ≥ 7 mmol/L before or after the acute episode.Group differences were tested by proportional hazards models in all-cause and cardiovascular mortality during a 7-year follow-up. Results: There were 188 (47%) patients without diabetes, 149 (37%) with clinical diabetes and 63 (16%) with undiagnosed diabetes. Patients with undiagnosed diabetes had a lower prevalence of hypertension, dyslipidaemia, peripheral vascular disease and previous myocardial infarction than those with clinical diabetes and similar to that of those without diabetes. The adjusted hazards ratios for 7-year total and cardiovascular mortality compared with the group of subjects without diabetes were 1.69 (95% CI: 1.17-2.46) and 2.45 (95% CI: 1.58-3.81) for those with undiagnosed diabetes, and 1.48 (95% CI: 1.10-1.99) and 2.01 (95% CI: 1.40-2.89) for those with clinical diabetes. Conclusions: Undiagnosed diabetes is common in patients requiring hospitalization for acute heart failure. Patients with undiagnosed diabetes, despite having a lower cardiovascular risk profile than those with clinical diabetes, show a similar increased mortality

Does long-term coffee intake reduce type 2 diabetes mellitus risk?

This review reports the evidence for a relation between long-term coffee intake and risk of type 2 diabetes mellitus. Numerous epidemiological studies have evaluated this association and, at this moment, at least fourteen out of eighteen cohort studies revealed a substantially lower risk of type 2 diabetes mellitus with frequent coffee intake. Moderate coffee intake (≥4 cups of coffee/d of 150 mL or ≥400 mg of caffeine/d) has generally been associated with a decrease in the risk of type 2 diabetes mellitus. Besides, results of most studies suggest a dose-response relation, with greater reductions in type 2 diabetes mellitus risk with higher levels of coffee consumption. Several mechanisms underlying this protective effect, as well as the coffee components responsible for this association are suggested. Despite positive findings, it is still premature to recommend an increase in coffee consumption as a public health strategy to prevent type 2 diabetes mellitus. More population-based surveys are necessary to clarify the long-term effects of decaffeinated and caffeinated coffee intake on the risk of type 2 diabetes mellitus

Comparison of glycemic excursion in patients with new onset type 2 diabetes mellitus before and after treatment with repaglinide

Due to industrialization and sedentary life, incidence of type 2 diabetes (DM2) is increasing seriously. Repaglinide is a glucose reducing agent that predominantly reduces post-prandial glucose. Continuous glucose monitoring system (CGMS) monitors blood glucose excursions over a 3-day period. CGMS can be used as a therapeutic and diagnostic instrument in diabetics. There are not enough studies about using CGMS in DM2. The aim of this study was to determine the blood glucose excursions in patients with new onset of DM2. 10 patients with new onset of DM2 were entered to this study. As the first therapeutic management, patients received diabetic diet and moderate exercise for 3-weeks, if they did not achieve blood glucose goal (Fasting blood glucoser (FBG) <120mg/dl, 2-hour postprandial blood glucose (2hpp) <180mg/dl), were considered to undergo 3-days CGMS at baseline and after 4-weeks on Repaglinide (0.5mg three times before meals). Mean excursions of blood glucose were not different at the onset and at the end of treatment (6±4.05 VS 7.6±5.2 episodes, P=0.49). There were also no significant differences between mean duration of hypoglycemic episodes (zero VS 5.1±14.1 hours, P =0.28) and hyperglycemic episodes before and after therapy (7.6±5.2 VS 5.7±4.1, P=0.42), but mean hyperglycemia duration was significantly reduced at the end of therapy (21±26.17 VS 57.7±35.3, P=0.001). Patients experienced a mean of 0.3±0.67 episodes of hypoglycemia after therapy showed no significant difference before it (P =0.19). Mean FBG (with CGMS) was significantly lower after therapy than before it (142.9±54.31 VS 222.9±82.6, P <0.001). This study showed the usefulness of CGMS not only as a diagnostic but also as an educational and therapeutic tool that in combination with Repaglinide (with the lowest effective dose and duration) can significantly reduce FBG and glycemic excursions in DM2 patients and hypoglycemic events are low. © Hezarkhani et al