The triglycerides and glucose index is more strongly associated with metabolically healthy obesity phenotype than the lipid and obesity indices.

PURPOSE: The triglycerides and glucose (TyG) index is a reliable biomarker for estimating insulin resistance; however, evidence regarding the use of the TyG index in individuals with metabolically healthy obesity (MHO) is scarce. Thus, we examined the association between the TyG index and the MHO phenotype. METHODS: Apparently healthy men and women aged 18 years or more with obesity (body mass index [BMI] ≥ 30 kg/m2) were allocated into the following groups: MHO and metabolically unhealthy obesity (MUO). The MHO phenotype was defined by obesity and the absence of the following metabolic disorders: elevated triglyceride concentrations, elevated glucose levels, elevated blood pressure, and low HDL-C. The MUO was defined by individuals with obesity and at least one of the aforementioned cardiovascular risk factors. RESULTS: A total 827 individuals, 605 (73.1%) women and 222 (26.9%) men were enrolled and allocated into the MHO (n = 104) and MUO (n = 723) groups. The adjusted regression analysis by age, sex, BMI, and waist circumference showed that fasting glucose (OR = 0.90; 95% CI: 0.88-0.93), and triglycerides (OR = 0.97; 95% CI: 0.96-0.98), as well as the triglycerides/HDL-C (OR = 0.18; 95% CI: 0.13-0.26), lipid accumulation product (OR = 0.95; 95% CI: 0.93-0.96), visceral adipose index (OR = 0.38; 95% CI: 0.31-0.46), and TyG index (OR = 0.001; 95% CI: 0.000-0.004) are inversely associated with the MHO, while the HDL-C (OR = 1.10; 95% CI: 1.07-1.12) had a direct association. CONCLUSIONS: Our results show that the TyG index is more strongly associated with the MHO phenotype than the lipid and obesity indices.

The triglycerides and glucose index is associated with cardiovascular risk factors in metabolically obese normal-weight subjects.

PURPOSE: The aim of this study was to determine whether the triglycerides and glucose (TyG) index is associated with the presence of metabolically obese normal-weight (MONW) phenotype and related cardiovascular risk factors. METHODS: Apparently healthy men and non-pregnant women aged 20-65 years were enrolled in a population-based cross-sectional study. Overweight, obesity, smoking, alcohol consumption, pregnancy, diagnosis of hypertension, diabetes, cardiovascular disease, liver disease, renal disease, malignancy, and medical treatment were exclusion criteria. Subjects were allocated into the MONW or normal-weight groups. MONW phenotype was defined by normal weight and the presence of at least one of the following cardiovascular risk factors: elevated blood pressure, hyperglycemia, hypertriglyceridemia, and low HDL cholesterol. RESULTS: A total of 542 subjects were enrolled and allocated into the MONW (n = 354) and normal-weight (n = 188) groups. The adjusted logistic regression analysis showed that the elevated TyG index is significantly associated with the presence of MONW phenotype (OR = 11.14; 95% CI 6.04-20.57), hyperglycemia (OR = 3.18; 95% CI 1.95-5.21), hypertriglyceridemia (OR = 399.19; 95% CI 94.01-1694.98), and low HDL-C (OR = 2.60; 95% CI 1.74-3.87), but not with elevated blood pressure (OR = 1.55; 95% CI 0.93-2.60). CONCLUSION: Results of this study support that the TyG index may be a useful indicator to detect MONW phenotype and associated cardiovascular risk factors.

The triglyceride and glucose index is useful for recognising insulin resistance in children.

AIM: Although recognising insulin resistance (IR) in children is particularly important, the gold standard test used to diagnose it, the euglyceamic glucose clamp, is costly, invasive and is not routinely available in our clinical settings in Mexico. This study evaluated whether the triglyceride-glucose (TyG) index would provide a useful alternative. METHODS: A total of 2779 school children aged seven to 17 years, from Durango, Mexico, were enrolled during 2015-2016. The gold standard euglyceamic-hyperinsulinemic clamp test was performed in a randomly selected subsample of 125 children, and diagnostic concordance between the TyG index and the homoeostasis model assessment of IR was evaluated in all of the 2779 enrolled children. RESULTS: The best cut-off values for recognising IR using the TyG index were 4.65 for prepubertal girls and boys, 4.75 for pubertal girls and 4.70 for pubertal boys. Concordance between the TyG index and the homoeostasis model assessment of IR was 0.910 and 0.902 for the prepubertal girls and boys, 0.932 for the pubertal girls and 0.925 for the pubertal boys. CONCLUSION: The TyG index was useful for recognising IR in both prepubertal and pubertal children and could provide a feasible alternative to the costly and invasive gold standard test for IR in resource-limited settings.

Effect of statin therapy on plasma proprotein convertase subtilisin kexin 9 (PCSK9) concentrations: a systematic review and meta-analysis of clinical trials.

AIMS: To evaluate the magnitude of the effect of statin therapy on plasma proprotein convertase subtilisin kexin 9 (PCSK9) levels through a systematic review and meta-analysis of clinical trials. METHODS: A random-effects model (using DerSimonian-Laird method) and the generic inverse variance method were used for quantitative data synthesis. Heterogeneity was quantitatively assessed using the I(2) index. Sensitivity analyses were conducted using the one-study remove approach. Random-effects meta-regression was performed using an unrestricted maximum likelihood method to evaluate the association between statin-induced elevation of plasma PCSK9 concentrations with duration of treatment and magnitude of LDL cholesterol reduction. RESULTS: A total of 15 clinical trials examining the effects of statin therapy on plasma PCSK9 levels were included. Meta-analysis of data from single-arm statin treatment arms [weighted mean difference (WMD) 40.72 ng/ml, 95% confidence interval (CI) 34.79, 46.65; p < 0.001] and randomized placebo-controlled trials (WMD 22.98 ng/ml, 95% CI 17.95, 28.01; p < 0.001) showed a significant increase in plasma PCSK9 concentrations after statin therapy, irrespective of the type of statin administered in either of the analyses (single-arm or randomized placebo-controlled trial). There was no significant elevation of plasma PCSK9 levels with statin/ezetimibe combination therapy compared with statin monotherapy (WMD 23.14 ng/ml, 95% CI -1.97, 48.25; p = 0.071); however, removal of one study in the meta-analysis yielded a significant result in the sensitivity analysis (WMD 31.41 ng/ml, 95% CI 7.86, 54.97; p = 0.009). CONCLUSIONS: This meta-analysis suggests that statin therapy causes a significant increase in plasma PCSK9 concentrations.

BORIS and CTCF are overexpressed in squamous intraepithelial lesions and cervical cancer.

We investigated the expression of Brother of Regulator of Imprinted Sites (BORIS) and CCCTC-binding factor (CTCF) in squamous intraepithelial lesions and cervical cancer. To analyze BORIS and CTCF expression, an endocervical cytobrush sample was taken for total RNA isolation. CTCF and BORIS mRNA was quantified from total RNA using quantitative reverse transcription-polymerase chain reaction. A total of 71 samples were collected and classified according to the Bethesda Classification of squamous intraepithelial lesions. BORIS expression was observed in 9 (12.7%) samples; of these, 5.3, 5.9, 14.8, and 37.5% in the groups that were cytology negative for intraepithelial lesion or malignancy, low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), and invasive cervical carcinoma, respectively. The expression level of BORIS was significantly higher in the group with invasive cervical carcinoma as compared with the groups negative for intraepithelial lesion or malignancy, LSIL, and HSIL (P < 0.0005). CTCF mRNA was expressed in all samples. CTCF expression was significantly higher in carcinoma groups compared with LSIL, HSIL, and negative for intraepithelial lesion or malignancy groups. We found that BORIS and CTCF expressions in the LSIL and invasive cervical carcinoma groups were higher than expression in cytological normal samples. Additional studies should be conducted to examine the function of transcription factors during different stages of the transformation of cervical cancer cells.

Tumor necrosis factor haplotype diversity in Mestizo and native populations of Mexico.

The so-called tumor necrosis factor (TNF) block includes the TNFA, lymphotoxin alpha and beta (LTA and LTB) genes with single-nucleotide polymorphisms (SNP) and microsatellites with an allele frequency that exhibits interpopulation variability. To date, no reports have included both SNPs and microsatellites at the TNF block to study Mestizo or Amerindian populations from Mexico. In this study, samples of five Mexican Mestizo populations (Durango, Guadalajara, Monterrey, Puebla, and Tierra Blanca) and four native-Mexican populations (North Lacandonians, South Lacandonians, Tepehuanos, and Yaquis) were genotyped for two SNPs (LTA+252A>G and TNFA-308G>A) and four microsatellites (TNFa, d, e, and f), to analyze the genetic substructure of the Mexican population. Allele and haplotype frequencies, linkage disequilibrium (LD), and interpopulation genetic relationships were calculated. There was significant LD along almost all of the TNF block but the lowest D' values were observed for the TNFf-TNFd pair. Mestizos showed higher allele and haplotype diversity than did natives. The genetic differentiation level was reduced among Mestizos; however, a slightly, but significant genetic substructure was observed between northern and southern Mexican Mestizos. Among the Amerindian populations, the genetic differentiation level was significantly elevated, particularly in both North and South Lacandonians. Furthermore, among Southern Lacandonians, inhabitants of Lacanja town were the most differentiated from all the Mexicans analyzed. The data presented here will serve as a reference for further population and epidemiological studies including these TNF polymorphisms in the Mexican population.

Dietary factors related to the increase of cardiovascular risk factors in traditional Tepehuanos communities from Mexico. A 10 year follow-up study.

BACKGROUND AND AIMS: Tepehuanos Indians, a traditional Mexican ethnic group, followed a vegetarian diet exhibiting a low prevalence of obesity and the absence of diabetes. However, from the year 2000 the traditional diet of the Tepehuanos was modified by the introduction of western food. In this study we examine the changes in their customary diet and its impact on the prevalence of cardiovascular risk factors in this group. METHODS AND RESULTS: Individuals from 12 Tepehuanos communities were randomly enrolled during 1995-1996 and 2006-2007. Using a 64-item semiquantitative food frequency questionnaire macronutrient intakes were calculated from values of Mexican food-composition tables. Cardiovascular risk factors such as obesity, hypertension, hyperglycemia and dyslipidemia were determined. The median (25, 75 percentile) of total caloric intake (1476 [1083, 1842]-2100 [1366, 2680]kcal/day, p<0.001) as well as the percentage of energy consumed from saturated fat (3.0 [2.7,4.1]-7.2 [3.9,7.4], p<0.0001) and protein (8.2 [7.8,8.9]-16.8 [16.3,17.1], p<0.0001) increased, whereas the percentage of total calorie intake from carbohydrates (66.4 [61.3,69.5]-61.3 [61,68.8], p<0.0001), polyunsaturated fat (11.2 [10.3,12.1]-4.0 [3.9,4.3], p<0.0001), and the polyunsaturated:saturated fat ratio (3.84-0.53%, p<0.0001) decreased during the period of study. The prevalence of obesity (11.1-21.9%, p=0.04), impaired fasting glucose (5.9-14.9%, p=0.04), diabetes (0.0-0.88%, p=0.48), hypertension (1.7-3.4%, p=0.43), triglycerides (2.6-16.7%, p=0.0006), and low HDL-cholesterol (10.2-71.1%, p<0.0001) increased. CONCLUSIONS: Changes in the customary diet introduced in the Tepehuanos communities are related to the increase of cardiovascular risk factors.

Hypomagnesaemia and risk for metabolic glucose disorders: a 10-year follow-up study.

BACKGROUND: Although several lines of evidence suggest that hypomagnesaemia is a risk factor for developing type 2 diabetes, there are no studies regarding the association between hypomagnesaemia and the risk for developing impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Our objective was to examine the association between serum magnesium levels and the risk for developing IFG, IGT and type 2 diabetes. MATERIALS AND METHODS: A total of 1122 individuals (20-65 years of age) were enrolled between 1996 and 1997, and 817 individuals re-examined about 10 years later. New-onset IFG (5.6-7.0 mmol L(-1) fasting glucose), IGT (7.8-11.1 mmol L(-1) glucose 2-h postload), and type 2 diabetes were determined from the number of subjects who had these conditions at the second examination without evidence that they were present at the first one. The relative risk of new-onset metabolic glucose disorders and diabetes (dependent variables) was computed using Poisson regression model adjusted for age, sex, family history of diabetes, waist circumference and homeostasis model assessment for insulin resistance index. Serum magnesium levels of < 0.74 mmol L(-1) (independent variable) defined the exposed group. RESULTS: At baseline, 420 (51.4%) individuals had hypomagnesaemia. New-onset IFG and IGT was identified in 276 (33.8%) individuals. The relative risk for IFG, IGT and IFG + IGT was 1.11 (95% confidence interval, 0.5-5.1), 1.38 (95% confidence interval, 1.1-6.3) and 1.49 (95% confidence interval, 1.1-4.9), respectively. New-onset diabetes was identified in 78 (9.5%) individuals (relative risk 2.54; 95% confidence interval, 1.1-4.1). CONCLUSIONS: Hypomagnesaemia is independently associated with the development of IGT, IFG + IGT and type 2 diabetes, but not with the development of IFG.

Effects of pentoxifylline on the urinary protein excretion profile of type 2 diabetic patients with microproteinuria: a double-blind, placebo-controlled randomized trial.

AIMS: The purpose of this study was to identify the effect of pentoxifylline on the urinary protein excretion profile in type 2 diabetic patients. METHODS: 40 type 2 nonhypertensive diabetic patients were randomly allocated to receive either pentoxifylline 400 mg t.i.d. or placebo daily for 16 weeks. Eligible subjects were those with urinary albumin excretion between 20 and 200 microg/min. Subjects receiving angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium antagonists, and diuretics as well as those with reduced renal function, pregnancy, urinary tract infection, and smoking were not included. A 6-month pretreatment stabilization phase aimed to reduce and stabilize fasting serum glucose levels was carried out. Urinary proteins were identified by electrophoresis, and immunodetection was identified by Western blot. Electrophoretic analysis was performed using molecular weight markers of 150, 132, 77, and 66 kDa to identify high-weight proteins, and 54, 41, 36, 27, 21, 14.3, and 12 kDa to identify low-weight proteins. RESULTS: At baseline, subjects in both groups who showed a glomerular tubular pattern did not differ in their urinary excretion profile. The urinary proteins identified were immunoglobulin G, ceruloplasmin, transferrin, and albumin (glomerular pattern) as well as alpha1-antitrypsin, alpha1-acid glycoprotein, collagenase inhibitor, alpha1-microglobulin, trypsin inhibitor, lysozyme, and beta2-microglobulin (tubular pattern). Subjects who received pentoxifylline had reduced urinary excretion of high- and low-molecular weight proteins. CONCLUSIONS: Urinary protein excretion in type 2 diabetic subjects shows a mixed, glomerular and tubular, pattern. Pentoxifylline reduces the excretion of both high and low molecular-weight urinary proteins.

Early decrease of the percent of HOMA beta-cell function is independently related to family history of diabetes in healthy young nonobese individuals.

OBJECTIVE: To determine the relationship between family history of diabetes (FHD) and decrease in percent of HOMA beta-cell function (HOMA-beta%) index in healthy betanon-obese Mexican subjects. MATERIALS AND METHODS: Forty-eight individuals (30 women and 18 men) with FHD were compared vs 48 control subjects (30 women and 18 men) in a cross-sectional study matched by age, sex, and Waist-to-Hip ratio. Pregnancy, obesity, being overweight, alcohol consumption, high blood pressure, and heavy physical activity were exclusion criteria. All the participants were required to have a Body Mass Index < 25 kg/m2 and serum fasting and 2-hours postload glucose levels lower than 6.1 mmol/l and 7.8 mmol/l, respectively. The reciprocal of serum fasting insulin concentrations (1/Ins0) (microU/ml) and HOMA-B% index were used as indicators of insulin sensitivity and beta-cell function. RESULTS: Average age was of 19.4 +/- 3.6 vs 19.8 +/- 2.6, P = 0.66 for the subjects with and without FHD. HOMA-beta% index was significantly lower in the subjects with FHD (186.1 +/- 74.1 vs 252.7 +/- 149.5, P = 0.01). For similar levels of insulin sensitivity, subjects with FHD showed lower HOMA-beta% index than control subjects (P < 0.001). Multivariate regression analysis showed a strong and independent relationship between FHD and decrease of HOMA-beta% index (OR 2.6, CI95% 1.2-4.3, P = 0.01). CONCLUSIONS: This study shows that normal-weight offspring of type 2 diabetes subjects exhibited a significant decrease of HOMA-beta% index suggesting that FHD exerts an independent early negative effect on beta-cell function.

Pentoxifylline is as effective as captopril in the reduction of microalbuminuria in non-hypertensive type 2 diabetic patients--a randomized, equivalent trial.

AIMS: To compare the efficacy of pentoxifylline and captopril on urinary albumin excretion (UAE) rate in non-hypertensive diabetic patients with microalbuminuria. METHODS: 450 subjects were screened; of these 130 eligible, non-hypertensive, type 2 diabetic subjects were enrolled and randomly allocated to receive either pentoxifylline 400 mg t.i.d. (n = 65) or captopril 25 mg t.i.d. (n = 65) for six months in a randomized equivalent trial design study. Patients were eligible to participate if they had microalbuminuria, defined by UAE rate of 20-200 microg/min, and systolic/diastolic blood pressure lower than 140/85 mmHg. Diagnosis of high blood pressure and renal failure were exclusion criteria. In addition, subjects receiving ACE inhibitors or pentoxifylline were not included. RESULTS: Both treatments were well tolerated, without serious adverse events; nonetheless, one subject (1.6%) in the group with pentoxifylline had severe headache, and three (4.7%) subjects in the group with captopril had intense dry cough and nasal congestion that required stopping pentoxifylline and captopril. In addition, slight headache and mild dry cough that did not require specific treatment or interruption of medication were present in two (3.2%) and five (7.8%) subjects treated with pentoxifylline and captopril. Four subjects dropped-out (one in the pentoxifylline group and three in the captopril group). Blood pressure and fasting glucose levels were similar between the two groups throughout the study. The UAE rate decreased from the first month of treatment in the subjects of both groups, a reduction that was sustained in the following months. At the end of the study, the average UAE rate in the subjects of both groups was lower than 25 microg/min. CONCLUSIONS: Pentoxifylline showed to be an effective alternative to ACE inhibitors in reducing UAE in non-hypertensive diabetic patients with microalbuminuria.

Oral magnesium supplementation improves glycaemic status in subjects with prediabetes and hypomagnesaemia: A double-blind placebo-controlled randomized trial.

AIM: This study evaluated the efficacy of oral magnesium supplementation in the reduction of plasma glucose levels in adults with prediabetes and hypomagnesaemia. METHODS: A total of 116 men and non-pregnant women, aged 30 to 65 years with hypomagnesaemia and newly diagnosed with prediabetes, were enrolled into a randomized double-blind placebo-controlled trial to receive either 30 mL of MgCl2 5% solution (equivalent to 382 mg of magnesium) or an inert placebo solution once daily for four months. The primary trial endpoint was the efficacy of magnesium supplementation in reducing plasma glucose levels. RESULTS: At baseline, there were no significant statistical differences in terms of anthropometric and biochemical variables between individuals in the supplement and placebo groups. At the end of follow-up, fasting (86.9 ± 7.9 and 98.3 ± 4.6 mg/dL, respectively; P = 0.004) and post-load glucose (124.7 ± 33.4 and 136.7 ± 23.9 mg/dL, respectively; P = 0.03) levels, HOMA-IR indices (2.85 ± 1.0 and 4.1 ± 2.7, respectively; P = 0.04) and triglycerides (166.4 ± 90.6 and 227.0 ± 89.7, respectively; P = 0.009) were significantly decreased, whereas HDL cholesterol (45.6 ± 10.9 and 46.8 ± 9.2 mg/dL, respectively; P = 0.04) and serum magnesium (1.96 ± 0.27 and 1.60 ± 0.26 mg/dL, respectively; P = 0.005) levels were significantly increased in those taking MgCl2 compared with the controls. A total of 34 (29.4%) people improved their glucose status (50.8% and 7.0% in the magnesium and placebo groups, respectively; P < 0.0005). CONCLUSION: Our results show that magnesium supplementation reduces plasma glucose levels, and improves the glycaemic status of adults with prediabetes and hypomagnesaemia.

Relation of C-reactive protein to features of the metabolic syndrome in normal glucose tolerant, impaired glucose tolerant, and newly diagnosed type 2 diabetic subjects.

OBJECTIVE: To determine the relationship between CRP levels and the components of MS in normal glucose tolerant (NGT), impaired glucose tolerant (IGT), and Type 2 diabetic subjects. MATERIAL AND METHODS: A based cross-sectional population study was performed. Eligible subjects, men and non-pregnant women, 30 to 64 year of age, were randomly recruited. Subjects with acute or chronic diseases were excluded. Only newly diagnosed type 2 diabetic or hypertensive subjects were included. Disorders related to CRP increase, also were exclusion criteria. In accordance to WHO proposal, components of MS were: High Blood Pressure, Dyslipidemia, Obesity, and Microalbuminuria, and MS was defined, for the NGT, if at least two of the criteria were fulfilled and in addition the subject had insulin resistance. The MS in IGT and DM subjects was defined if at least two of the criteria were fulfilled. RESULTS: CRP was significantly associated with MS for the NGT (Odds ratio -OR- 3.8, CI(95%) 1.6-14.8), IGT (OR 4.9, CI(95%) 1.2-15.5), and diabetes (OR 5.6, CI(95%) 1.9-10.2). For NGT, after adjustment for obesity, CRP was not longer associated with MS. After adjust for obesity and fasting glucose (FG), the relationship between CRP and MS for IGT was lost. Finally, after adjustment for obesity, FG, and microalbuminuria, CRP was not longer associated with MS for diabetic subjects. CONCLUSIONS: This study show a significant relationship between CRP and MS which is maintained only by obesity in the NGT, by obesity and FG in the IGT, and by obesity, FG, and microalbuminuria in the newly diagnosed diabetic subjects.

Glucose intolerance is predicted by the high Fasting Insulin-to-Glucose ratio.

OBJECTIVE: To determine whether impaired glucose tolerance (IGT) is predicted by high Fasting Insulin-to-Glucose (FIG) ratio and to establish its correlation with insulin resistance and fasting insulin. MATERIAL AND METHODS: A population-based three-year follow-up study was performed. The target population consisted of healthy volunteers, men and non-pregnant women aged 30 years or over. Participants were required to have normal referenced ranges of OGTT and blood pressure. Previous diagnosis of chronic diseases was an exclusion criterion. At baseline and at the 3-yr of follow-up, an OGTT was performed. The ratio of serum Fasting Insulin (microUI/ml)/Fasting Glucose (mg/dl) was used to calculate the FIG ratio. Insulin action and secretion were estimated by HOMA and Insulinogenic index, respectively. RESULTS: The FIG ratio was directly correlated with the HOMA index (r=0.83, p<0.01) and fasting insulin (r=0.95, p<0.001). Multivariate logistic regression analysis showed that IGT was more likely to develop in subjects with high FIG ratio (RR 5.01; CI(95%) 1.9-12.2, p=0.02), high HOMA index (RR 6.1; CI(95%) 2.1-11.1, p=0.01), and fasting hyperinsulinemia (RR 4.7 CI(95%) 2.7-13.2, p<0.05). The cutoff point of FIG ratio for determining the risk of developing IGT was 0.25 +/- 0.05. CONCLUSIONS: The FIG ratio could be a reliable alternative for the screening of apparently healthy subjects in high risk groups.

Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial.

OBJECTIVE: Although hypomagnesemia reduces insulin sensitivity, benefits of magnesium supplementation to non-diabetic insulin resistant subjects has not been established. Our purpose was to determine whether oral magnesium supplementation with magnesium chloride (MgCl2) 2.5 g daily modify insulin sensitivity in non-diabetic subjects. MATERIAL AND METHODS: This study was a 3 months randomized double-blind placebo-controlled trial. Apparently healthy subjects were eligible to participate if they had insulin resistance (HOMA-IR index equal or greater than 3.0) and hypomagnesemia (Serum magnesium levels equal or lower than 0.74 mmol/l). Subjects were randomized to receive either, MgCl2 2.5 g daily or placebo by 3-months. RESULTS: At baseline there were not significant anthropometric or laboratory differences between both groups. At ending of the study, magnesium-supplemented subjects significantly increased their serum magnesium levels (0.61 +/- 0.08 to 0.81 +/- 0.08 mmol/l, p<0.0001) and reduced HOMA-IR index (4.6 +/- 2.8 to 2.6 +/- 1.1, p<0.0001), whereas control subjects did not (0.62 +/- 0.08 to 0.61 +/- 0.08 mmol/l, p=0.063 and 5.2 +/- 1.9 to 5.3 +/- 2.9, p=0.087). CONCLUSIONS: Oral magnesium supplementation improves insulin sensitivity in hypomagnesemic non-diabetic subjects. Clinical implications of this finding have to be established.

Prevalence of hypertension in indigenous inhabitants of traditional communities from the north of Mexico.

The purpose of this study was to estimate the prevalence and risk factors of hypertension in adults indigenous to their traditional communities from the north of Mexico. The study was based on a cross- sectional survey of inhabitants from Mexicaneros, Huicholes and Tepehuanos communities, which have not been influenced by a western lifestyle. A home interview and clinical examination that included blood pressure and anthropometric measurements of 217 men and 598 non-pregnant women aged between 35 to 64 years was carried out. Eligible indigenous subjects must have had no migratory history to partially or totally urbanised areas. Target population represented approximately 100% of the indigenous people who have spent all their life time in the community of birthplace. Age and body mass index average was 48.9+/-12.9 years and 25.6+/-5.1 kg/m2. Hypertension was identified in 56 individuals, 45 women and 11 men (prevalence 6.87%, 95% confidence interval (CI) 5.1-8.6). Forty-one percent of the hypertensive subjects were aware of being hypertensive. Hypertensive subjects had a higher intake of saturated fats than non-hypertensives. Salt consumption was lower than 6 g per day in subjects with and without hypertension. High intake of saturated fats (odds ratio 6.4, 95% CI 2.1-12.3; P<0.01) was an independent predictor for hypertension. This study presents, for the first time, data concerning hypertension in adults who are indigenous to and living in traditional communities from Mexico. Prevalence of hypertension was lower than in the partly urbanised rural communities with a westernised lifestyle and the urban areas of Mexico.

Hyperinsulinemia and abdominal obesity are more prevalent in non-diabetic subjects with family history of type 2 diabetes.

BACKGROUND: This study was undertaken in order to identify the relationships between family history of type 2 diabetes and cardiovascular risk factors in non-diabetic Mexican individuals. METHODS: The design was a cross-sectional, population-based study stratified by age and sex. Participants consisted of 189 non-diabetic volunteers 30-64 years of age, both males and non-pregnant females randomly selected from a middle income neighborhood in Durango, Mexico and distributed into two groups, with and without family history of type 2 diabetes mellitus. Hypertensive subjects were excluded. Body mass index (BMI) and waist-to-hip ratio (WHR) were assessed. Hematocrit, both fasting and 2-h post 75-g glucose load insulin, and glucose levels, lipid profile, serum albumin, and proteinuria were measured. RESULTS: Ninety-four (49.7%) individuals with family history of type 2 diabetes, and 95 (50.3%) in the control group were included. The prevalence of obesity was greater among women with family history of diabetes, 39 (73.6%) vs. 27 (50.0%) of the control group, p = 0.02. Adiposity tended to be centrally distributed in 86 subjects, of whom 22 (25. 6%) males and 54 (62.8%) females were in the group with family history of diabetes and four (4.6%) males and six (7.0%) females in the control group, p <0.000. Multivariate logistic regression analysis showed a strong relationship between family history of type 2 diabetes with both abdominal obesity (odds ratio [OR] 4.2, CI 95% 1.9-10.1, p <0.05) and fasting hyperinsulinemia (OR 3.1, CI 95% 1. 4-11.2, p <0.05). CONCLUSION: In the absence of additional risk factors such as diabetes and hypertension, there is a strong relationship between family history of diabetes with hyperinsulinemia and abdominal obesity in middle-aged Mexican individuals.

Low serum magnesium levels and foot ulcers in subjects with type 2 diabetes.

BACKGROUND: Hypomagnesemia is associated with the development of neuropathy and abnormal platelet activity, both of which are risk factors for the progression of ulcers of the feet. Thus, the aim of this study was to determine the relationship between low serum magnesium and foot ulcer in subjects with type 2 diabetes. METHODS: Thirty-three out-patients with type 2 diabetes and foot ulcers (16 women and 17 men) were compared with a control group of 66 out-patients with type 2 diabetes without foot ulcers (35 women and 31 men), matched by age, diabetes duration, HbA1c, and glycemia. Patients with foot ulcers were included in the study only if a foot ulceration onset not exceeding 2 months was established. Patients diagnosed with reduced renal function, a history of alcohol intake, or as having received magnesium supplementation or diuretics were not included. Serum magnesium was measured by colorimetric method. The relationship between serum magnesium and foot ulcers was assessed by logistic regression. RESULTS: Hypomagnesemia was identified in 31 (93.9%) subjects with foot ulcers, and 49 (73.1%) control subjects, p = 0.02. Subjects with foot ulceration had lower serum magnesium levels (1.48 +/- 0.33) than those in the control group (1.68 +/- 0.32), p <0.001. Logistic regression analysis showed a significant relationship between low serum magnesium levels and foot ulcers (odds ratio [OR] 2.9, CI 95% 1.7-6.8; p = 0.01). CONCLUSIONS: Serum magnesium depletion is present and shows a strong relationship with foot ulcers in subjects with type 2 diabetes and foot ulcers, a relationship not previously reported.

Low prevalence of non-insulin-dependent diabetes mellitus in indigenous communities of Durango, Mexico.

To determine the prevalence and associated risk factors of non-insulin-dependent diabetes mellitus (NIDDM) in inhabitants of traditional indigenous communities from Durango, Mexico, a transversal descriptive study was conducted. Tepehuano, Huichol and Mexicanero tribe members without racial admixture and a minimal Western influence on lifestyle were studied. One hundred and ninety-three subjects were included, this figure corresponding to approximately 20% of subjects aged from 30 to 64 years of the target population. Glycemia was determined in capillary blood after an overnight fast of 10-12 h, and 2 h after a 75 g oral glucose load using a Glucometer II device; NIDDM diagnosis was established according to the WHO criteria. Personal risk factors of NIDDM were determined. The average glucose level was 87.5 +/- 19.3 mg/dl. There were no NIDDM cases, hence the prevalence was 0.0%. The personal risk factors profile for NIDDM were as follows: 0.0% of cases with family history of NIDDM and with residency in urban areas > 40% of their lifetime, 7.2% of obese subjects and 15.5% of subjects with alcohol intake > or = 8 g/day. The absence of NIDDM suggests that this disease may be rare in traditional indigenous communities of Mexico and may be associated with less exposure to risk factors or genetic differences.

Pioglitazone increases serum magnesium levels in glucose-intolerant subjects. A randomized, controlled trial.

Although thiazolidinediones and magnesium supplementation improves insulin action and increases HDL-cholesterol, the potential link between serum magnesium and thiazolidinediones has received little attention. Focusing on the increase of serum magnesium, 63 eligible subjects were enrolled and randomly allocated to receive either 30 mg Pioglitazone once daily (Group A) or lifestyle intervention (Group B) during 12 weeks. Subjects were eligible if they were glucose-intolerant, and excluded if they had high blood pressure, diabetes or abnormal liver function tests. The personnel assessing outcomes were blinded to group assignment. Of the 63 eligible subjects, 3 dropped out (one in group A, and two in Group B) because they moved out of the city. So, 30 subjects in each group, who satisfactorily completed the follow-up, were included in the analysis of data. There were no serious adverse events or side effects due to Pioglitazone or lifestyle intervention. At baseline, the groups did not differ significantly in serum magnesium levels 1.73 +/- 0.17 versus 1.72 +/- 0.14 mg/dl, p = 0.80. Subjects who received Pioglitazone significantly increased their serum magnesium to 1.93 +/- 0.16 mg/dl whereas in the lifestyle intervention group the increase was 1.74 +/- 0.25 mg/dl, p < 0.0001. What this study showed was a significant increase in the serum magnesium levels of glucose-intolerant subjects who received 30 mg Pioglitazone once daily.