A dietary pattern including nopal, chia seed, soy protein, and oat reduces serum triglycerides and glucose intolerance in patients with metabolic syndrome.

Metabolic syndrome (MetS) is a health problem throughout the world and is associated with cardiovascular disease and diabetes. Thus, the purpose of the present work was to evaluate the effects of a dietary pattern (DP; soy protein, nopal, chia seed, and oat) on the biochemical variables of MetS, the AUC for glucose and insulin, glucose intolerance (GI), the relationship of the presence of certain polymorphisms related to MetS, and the response to the DP. In this randomized trial, the participants consumed their habitual diet but reduced by 500 kcal for 2 wk. They were then assigned to the placebo (P; n = 35) or DP (n = 32) group and consumed the reduced energy diet plus the P or DP beverage (235 kcal) minus the energy provided by these for 2 mo. All participants had decreases in body weight (BW), BMI, and waist circumference during the 2-mo treatment (P < 0.0001); however, only the DP group had decreases in serum TG, C-reactive protein (CRP), and AUC for insulin and GI after a glucose tolerance test. Interestingly, participants in the DP group with MetS and the ABCA1 R230C variant had a greater decrease in BW and an increase in serum adiponectin concentration after 2 mo of dietary treatment than those with the ABCA1 R230R variant. The results from this study suggest that lifestyle interventions involving specific DP for the treatment of MetS could be more effective if local foods and genetic variations of the population are considered.

Sucralose Consumption over 2 Weeks in Healthy Subjects Does Not Modify Fasting Plasma Concentrations of Appetite-Regulating Hormones: A Randomized Clinical Trial.

BACKGROUND: The effect of nonnutritive sweeteners on appetite is controversial. Some studies have found changes in certain appetite control hormones with sucralose intake that may be through interaction with sweet taste receptors located in the intestine. OBJECTIVE: The aim of this study was to evaluate whether sucralose consumption could produce changes in fasting plasma concentrations of appetite-regulating hormones, including glucagon-like peptide 1, ghrelin, peptide tyrosine tyrosine, and leptin, and secondarily in insulin resistance. DESIGN: A 2-week parallel randomized clinical trial with an additional visit conducted 1 week after dosing termination. PARTICIPANTS/SETTING: Sixty healthy, normal-weight individuals, without habitual consumption of nonnutritive sweeteners were recruited from July 2015 to March 2017 in Mexico City. INTERVENTION: Daily sucralose consumption at 15% of the acceptable daily intake by using commercial sachets added to food. The control group followed the same protocol without an intervention. MAIN OUTCOMES MEASURED: Fasting concentrations of appetite regulating hormones before and after the intervention. Fasting glucose and insulin concentrations were measured to assess insulin resistance as a secondary outcome. STATISTICAL ANALYSIS PERFORMED: Basal and final concentrations were compared using Wilcoxon matched-pairs test and Mann-Whitney U test for analysis between groups. Repeated measures analysis of variance was used to evaluate changes in the homeostasis model assessment of insulin resistance. RESULTS: Sucralose was not associated with changes in any of the hormones measured. One week postintervention, an incremental change (P=0.04) in the homeostasis model assessment of insulin resistance was found in the intervention group. CONCLUSIONS: Sucralose intake is not associated with changes in fasting concentrations of glucagon-like peptide 1, ghrelin, peptide tyrosine tyrosine, or leptin. An increase in the homeostasis model assessment of insulin resistance observed only at 1 week postdosing is of unknown clinical significance, if any.

The SLC16A11 risk haplotype is associated with decreased insulin action, higher transaminases and large-size adipocytes.

Objective A haplotype at chromosome 17p13 that reduces expression and function of the solute carrier transporter SLC16A11 is associated with increased risk for type 2 diabetes in Mexicans. We aim to investigate the detailed metabolic profile of SLC16A11 risk haplotype carriers to identify potential physiological mechanisms explaining the increased type 2 diabetes risk. Design Cross-sectional study. Methods We evaluated carriers (n = 72) and non-carriers (n = 75) of the SLC16A11 risk haplotype, with or without type 2 diabetes. An independent sample of 1069 subjects was used to replicate biochemical findings. The evaluation included euglycemic-hyperinsulinemic clamp, frequently sampled intravenous glucose tolerance test (FSIVGTT), dual-energy X-ray absorptiometry (DXA), MRI and spectroscopy and subcutaneous abdominal adipose tissue biopsies. Results Fat-free mass (FFM)-adjusted M value was lower in carriers of the SLC16A11 risk haplotype after adjusting for age and type 2 diabetes status (ß = -0.164, P = 0.04). Subjects with type 2 diabetes and the risk haplotype demonstrated an increase of 8.76 U/L in alanine aminotransferase (ALT) (P = 0.02) and of 7.34 U/L in gamma-glutamyltransferase (GGT) (P = 0.05) compared with non-carriers and after adjusting for gender, age and ancestry. Among women with the risk haplotype and normal BMI, the adipocyte size was higher (P < 0.001). Conclusions Individuals carrying the SLC16A11 risk haplotype exhibited decreased insulin action. Higher serum ALT and GGT levels were found in carriers with type 2 diabetes, and larger adipocytes in subcutaneous fat in the size distribution in carrier women with normal weight.

High adiponectin concentrations are associated with the metabolically healthy obese phenotype.

CONTEXT: In the ob/ob mice, keeping adiponectin concentrations in the physiological range (through overexpression of this gene in the adipose tissue) results in expansion of fat mass and protection against metabolic co-morbidities. OBJECTIVE: The aim of the study was to test in humans whether plasma adiponectin levels, similar to those found in lean subjects, are associated with the metabolically healthy obese phenotype. DESIGN AND SETTING: A cross-sectional analysis was performed of a cohort of obese and nonobese subjects aged 18-70 yr. A medical history was taken, and glucose, plasma lipids, and total adiponectin were measured. PARTICIPANTS: We studied 189 men and 527 women. The majority were obese (n = 470, 65.6%). The metabolically healthy obese phenotype was found in 38 men and 133 women. This is defined as a body mass index (BMI) above 30 kg/m(2) plus high-density lipoprotein cholesterol of at least 40 mg/dl in the absence of type 2 diabetes and arterial hypertension. RESULTS: Twenty percent of the cases with a BMI above 40 kg/m(2) had adiponectin concentrations above the median value of normal BMI subjects. Adiponectin levels above 12.49 mg/liter in obese women (odds ratio, 3.02; 95% confidence interval, 1.95-4.67; P < 0.001) and above 8.07 mg/liter in obese men (odds ratio, 2.14; 95% confidence interval, 1.1-4.06; P = 0.01) increased the probability of being metabolically healthy. The association remained significant (beta, 0.673 +/- 0.205, P < 0.001) in a logistic regression model (r(2) = 0.25, P < 0.001) after controlling for the confounding effect of age, insulin, and waist circumference. CONCLUSIONS: Certain obese individuals have adiponectin levels similar to those found in normal BMI subjects; this is associated with the metabolically healthy obese phenotype.

Lack of agreement between the plasma lipid-based criteria and apoprotein B for the diagnosis of familial combined hyperlipidemia in members of familial combined hyperlipidemia kindreds.

Our objective was to analyze the concordance between abnormally high-cholesterol and triglyceride concentrations and increased apoliprotein B (apoB) concentrations for considering subjects as affected in familial combined hyperlipidemia (FCHL) kindreds. Twenty-two FCHL families (n = 217) were included. There was a lack of agreement in the identification of the abnormal subjects when several cholesterol- and triglyceride-based criteria were compared against various apoprotein B-based criteria. The agreement, measured as kappa coefficients, between 14 lipid-based criteria and 8 apoB concentrations is reported. For the most frequently used criterion (> or = 90th percentile for cholesterol or triglyceride concentrations), the agreement was low for all apoB levels (kappa, 0.42 to 0.49). A concentration of triglycerides > or = 150 mg/dL and cholesterol > or = 200 mg/dL was the only criterion with a kappa value above 0.6; the acceptable agreement was found with an apoB concentration > or = 120 mg/dL (kappa = 0.604). In conclusion, the data reported here clearly show that a large degree of diagnostic uncertainty exists in the categorization as normal or abnormal of members of FCHL kindred. Different diagnostic criteria would result in conflicting results. This is a critical issue, depending on the diagnostic criteria used, completely different conclusions could result from the linkage analysis in the FCHL studies.

Association of the I148M/PNPLA3 variant with elevated alanine transaminase levels in normal-weight and overweight/obese Mexican children.

BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) and elevated alanine transaminase (ALT) levels are common in obese Hispanic adults and children. Recently, a PNPLA3 gene variant (I148M) was strongly associated with NAFLD and higher ALT levels in obese adults, including Hispanics. The aims of this study were to estimate the frequency of elevated ALT levels, and to address the influence of obesity and PNPLA3/I148M on ALT levels in a general population sample of Mexican school-aged children. METHODS: A total of 1037 non-related Mexican children aged 6 to 12 years were genotyped for the I148M variant. Anthropometric, clinical and metabolic parameters were collected from all participants. RESULTS: Elevated ALT levels (>35 U/L) were more frequent in obese (26.9%) and overweight (9.3%) than in normal weight children (2.2%). The M148M genotype was significantly associated with elevated ALT levels in this population (OR=3.7, 95% CI 2.3-5.9; P=3.7×10(-8)), and children carrying the M148M genotype showed significantly lower HDL cholesterol levels and BMI z-core (P=0.036 and 0.015, respectively). On stratifying by BMI percentile, this genotype conferred a much greater risk of elevated ALT levels in normal weight (OR=19.9, 95% CI 2.5-157.7; P=0.005) than overweight and obese children (OR=3.4, 95% CI 1.3-8.9; P=0.014 and OR=3.1, 95% CI 1.7-5.5; P=1.4 x10(-4), respectively). CONCLUSIONS: The I148M PNPLA3 variant is strongly associated with elevated ALT levels in normal weight and overweight/obese Mexican children. Thus, the M148M genotype may be considered as an important risk factor for liver damage in this population.