High Dietary Magnesium Intake is Significantly and Independently Associated with Higher Insulin Sensitivity in a Mexican-Mestizo Population: A Brief Cross-Sectional Report.

BACKGROUND: Magnesium acts as a cofactor in many intracellular reactions including phosphorylation of the insulin receptor; therefore, its imbalance can potentially cause insulin resistance. Low serum magnesium concentration has been associated with the development of metabolic syndrome and type 2 diabetes mellitus. OBJECTIVE: To study the association between the daily dietary magnesium intake and insulin resistance estimated by the homeostatic model assessment of insulin resistance and homeostatic model assessment 2, as well as insulin sensitivity estimated by the Matsuda index. METHODS: In a university affiliated medical center, 32 participants (22 women, 10 men) that had an indication for testing for type 2 diabetes mellitus with an oral glucose tolerance test were enrolled in this cross-sectional, comparative study. Clinical and biochemical evaluations were carried out including an oral glucose tolerance test. Hepatic insulin resistance index, homeostatic model assessment 2, homeostatic model assessment of insulin resistance, and Matsuda insulin sensitivity were calculated for each participant. They were asked to recall their food ingestion (24 hours) of three days of the past week, including a weekend day; magnesium intake was calculated according to the food nutritional information. RESULTS: The low dietary magnesium intake group (< 4.5 mg/kg/day) had a higher two-hour insulin concentration after an oral glucose tolerance test compared to those with high dietary magnesium (119.5 [73.0-190.6] vs. 63.5 [25.4-114.2]; p = 0.008), and insulin sensitivity assessed by the Matsuda index was higher in the high dietary magnesium intake group (4.3 ± 3.1 vs. 2.4 ± 1.5; p = 0.042). In multiple linear regression analysis a higher dietary magnesium intake was independently associated (ß = 4.93; p = 0.05) with a better insulin sensitivity estimated by the Matsuda index. CONCLUSIONS: Our results suggest that higher magnesium intake is independently associated with better insulin sensitivity in patients at risk for type 2 diabetes mellitus.

Effect of tomato consumption on high-density lipoprotein cholesterol level: a randomized, single-blinded, controlled clinical trial.

INTRODUCTION: Epidemiologic evidence suggests that tomato-based products could reduce the risk of cardiovascular diseases. One of the main cardiovascular risk factors is low levels of high-density lipoprotein cholesterol (HDL-C). This study aimed to prospectively evaluate the effect of tomato consumption on HDL-C levels. SUBJECT AND METHODS: We conducted a randomized, single-blinded, controlled clinical trial. We screened 432 subjects with a complete lipid profile. Those individuals with low HDL-C (men <40 mg/dL and women <50 mg/dL) but normal triglyceride levels (<150 mg/dL) were included. Selected participants completed a 2-week run-in period on an isocaloric diet and then were randomized to receive 300 g of cucumber (control group) or two uncooked Roma tomatoes a day for 4 weeks. RESULTS: A total of 50 individuals (women = 41; 82%) with a mean age of 42 ± 15.5 years and a mean body mass index of 27.6 ± 5.0 kg/m(2) completed the study. A significant increase in HDL-C levels was observed in the tomato group (from 36.5 ± 7.5 mg/dL to 41.6 ± 6.9 mg/dL, P < 0.0001 versus the control group). After stratification by gender, the difference in HDL-C levels was only significant in women. The mean HDL-C increase was 5.0 ± 2.8 mg/dL (range 1-12 mg/dL). Twenty patients (40%) finished the study with levels >40 mg/dL. A linear regression model that adjusted for those parameters that impact HDL-C levels (age, gender, waist-to-hip ratio, body mass index, fasting triglyceride concentration, simple sugars, alcohol, physical activity, and omega-3 consumption) showed an independent association between tomato consumption and the increase in HDL-C (r (2) = 0.69; P < 0.0001). CONCLUSION: Raw tomato consumption produced a favorable effect on HDL-C levels in overweight women.

Association of Alanine Aminotransferase Levels (ALT) with the Hepatic Insulin Resistance Index (HIRI): a cross-sectional study.

BACKGROUND: The association between serum alanine aminotransferase (ALT) levels and hepatic insulin resistance (IR) has been evaluated with the hyperinsulinemic-euglycemic clamp. However, there is no information about the association of ALT with the Hepatic Insulin Resistance Index (HIRI). The aim of this study was to evaluate the association between serum ALT levels and HIRI in subjects with differing degrees of impaired glucose metabolism. METHODS: This cross-sectional study included subjects that had an indication for testing for type 2 diabetes mellitus (T2DM) with an oral glucose tolerance test (OGTT). Clinical and biochemical evaluations were carried out including serum ALT level quantification. HIRI was calculated for each participant. Correlation analyses and lineal regression models were used to evaluate the association between ALT levels and HIRI. RESULTS: A total of 324 subjects (37.6% male) were included. The mean age was 40.4 ± 14.3 years and the mean body mass index (BMI) was 32.0 ± 7.3 kg/m2. Individuals were divided into 1 of 5 groups: without metabolic abnormalities (n = 113, 34.8%); with the metabolic syndrome (MetS, n = 179, 55.2%), impaired fasting glucose (IFG, n = 85, 26.2%); impaired glucose tolerance (IGT, n = 91, 28.0%), and T2DM (n = 23, 7.0%). The ALT (p < 0.001) and HOMA2-IR (p < 0.001) values progressively increased with HIRI quartiles, while ISI-Matsuda (p < 0.001) progressively decreased. After adjustment for sex, age, and BMI, we identified a significant correlation between HIRI and ALT in persons with the MetS (r = 0.22, p = 0.003), IFG (r = 0.33, p < 0.001), IGT (r = 0.37, p < 0.001), and T2DM (r = 0.72, p < 0.001). Lineal regression analysis adjusting for age, HDL-C, TG and waist circumference (WC) showed an independent association between ALT and HIRI in subjects with the MetS (beta = 0.07, p = 0.01), IFG (beta = 0.10, p = 0.02), IGT (beta = 0.09, p = 0.007), and T2DM (beta = 0.31, p = 0.003). This association was not identified in subjects without metabolic abnormalities. CONCLUSIONS: ALT levels are independently associated with HIRI in subjects with the MetS, IFG, IGT, and T2DM. The ALT value in these subjects may be an indirect parameter to evaluate hepatic IR.

Exercise increases serum fibroblast growth factor 21 (FGF21) levels.

BACKGROUND: Fibroblast growth factor 21 (FGF21) increases glucose uptake. It is unknown if FGF21 serum levels are affected by exercise. METHODOLOGY/PRINCIPAL FINDINGS: This was a comparative longitudinal study. Anthropometric and biochemical evaluation were carried out before and after a bout of exercise and repeated after two weeks of daily supervised exercise. The study sample was composed of 60 sedentary young healthy women. The mean age was 24±3.7 years old, and the mean BMI was 21.4±7.0 kg/m². The anthropometric characteristics did not change after two weeks of exercise. FGF21 levels significantly increased after two weeks of exercise (276.8 ng/l (142.8-568.6) vs. (460.8 (298.2-742.1), p<0.0001)). The delta (final-basal) log of serum FGF21, adjusted for BMI, showed a significant positive correlation with basal glucose (r = 0.23, p = 0.04), mean maximal heart rate (MHR) (r = 0.54, p<0.0001), mean METs (r = 0.40, p = 0.002), delta plasma epinephrine (r = 0.53, p<0.0001) and delta plasma FFAs (r = 0.35, p = 0.006). A stepwise linear regression model showed that glucose, MHR, METs, FFAs, and epinephrine, were factors independently associated with the increment in FGF21 after the exercise program (F = 4.32; r²â€Š= 0.64, p<0.0001). CONCLUSIONS: Serum FGF21 levels significantly increased after two weeks of physical activity. This increment correlated positively with clinical parameters related to the adrenergic and lipolytic response to exercise. TRIAL REGISTRATION: ClinicalTrials.gov NCT01512368.

Metformin and improvement of the hepatic insulin resistance index independent of anthropometric changes.

OBJECTIVE: To determine the change in the hepatic insulin resistance index (HIRI) after metformin treatment. METHODS: In this retrospective cohort study, Mexican mestizo patients with a body mass index (BMI) of 25 kg/m(2) or greater were evaluated. Participants were classified into 2 groups: patients who received metformin and patients who did not. Both groups were followed up for a median of 6 months (range, 4-10 months). The HIRI was calculated at baseline and at follow-up in both groups. We evaluated the independent effect of metformin on HIRI after adjustment for the difference in basal and final values (DELTA) of BMI, waist circumference, glucose, and insulin. RESULTS: A total of 71 patients were enrolled (51 [72%] female). Forty-one patients received metformin and 30 patients did not. Mean age was 36.3 ± 12.2 years and mean BMI was 42.2 ± 10.7 kg/m(2). After metformin treatment, HIRI significantly decreased from 38 ± 10.7 to 34.7 ± 9.5 (P = .03). In contrast, the control group had a nonsignificant increase in HIRI (37.6 ± 11.7 to 40.0 ± 14.0, P = .22). Weight significantly decreased in both groups (group 1: 114.6 ± 33.8 kg to 107.6 ± 28.9 kg, P<.01; group 2: 104.8 ± 28.5 kg to 98.9 ± 26.0 kg, P<.01). After BMI adjustment, the total metformin dosage correlated negatively with HIRI (r = -0.36, P = .03). Using a linear regression model (F = 6.0, r2 = 0.37, P = .002) adjusted for DELTA BMI and DELTA waist circumference, the administration of metformin resulted in independent improvement in the HIRI level (standardized ß = -0.29, t = -2.0, P = .04). CONCLUSIONS: Metformin improves HIRI independently of anthropometric changes. In persons with elevated HIRI levels, metformin may be considered among the treatment options.

Daily physical activity, fasting glucose, uric acid, and body mass index are independent factors associated with serum fibroblast growth factor 21 levels.

OBJECTIVE: Fibroblast growth factor 21 (FGF21) levels have been linked with beneficial effects on glucose and lipid metabolism in animals. It is elevated in humans with the metabolic syndrome. This study investigates independent factors associated with serum FGF21 levels. DESIGN: Cross-sectional study done in healthy blue-collar workers. METHODS: A medical history was taken, and FGF21 (measured using an ELISA commercial kit), glucose, uric acid, plasma lipids, total/high-molecular weight (HMW) adiponectin, and retinal-binding protein 4 (RBP4) were measured in 210 individuals with (n=81) and without (n=129) metabolic syndrome. RESULTS: The median of serum FGF21 levels were higher in subjects with metabolic syndrome (339.5 vs 276.4 ng/l, P=0.01). Serum FGF21 levels correlated positively with body mass index (BMI; r=0.23, P=0.001) and age (r=0.17, P=0.01). After adjusting for age and BMI, a significant positive correlation persisted for fasting glucose, uric acid, and physical activity in both males (r=0.21, r=0.11, and r=0.19, all P<0.05) and females (r=0.20, r=0.19, and r=0.14, all P<0.05). In addition, FGF21 also correlates negatively with RBP4 (r=-0.27, P=0.02), total (r=-0.26, P=0.03), and HMW adiponectin (r=-0.30, P=0.01) in women. A multiple linear regression model analysis identified that BMI (standardized beta (SB)=0.247; P=0.008), glucose (SB=0.226; P=0.003), uric acid (SB=0.191; P=0.04), and physical activity (SB=0.223; P=0.004) are independent factors influencing serum FGF21 levels (F=10.05, r(2)=0.19, P<0.001). In addition, fasting hyperglycemia > or =100 mg/dl, excess body weight with BMI > or =25 kg/m(2), and uric acid > or =5.5 mg/dl predicted higher serum FGF21 levels. CONCLUSION: Serum FGF21 levels are influenced by BMI, fasting glycemia, uric acid, and physical activity.