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Altered methionine metabolism is associated with weight gain in obesity. The methionine adenosyltransferase (MAT), catalyzing the first reaction of the methionine cycle, plays an important role regulating lipid metabolism. However, its role in obesity, when a plethora of metabolic diseases occurs, is still unknown. By using antisense oligonucleotides (ASO) and genetic depletion of Mat1a, here, we demonstrate that Mat1a deficiency in diet-induce obese or genetically obese mice prevented and reversed obesity and obesity-associated insulin resistance and hepatosteatosis by increasing energy expenditure in a hepatocyte FGF21 dependent fashion. The increased NRF2-mediated FGF21 secretion induced by targeting Mat1a, mobilized plasma lipids towards the BAT to be catabolized, induced thermogenesis and reduced body weight, inhibiting hepatic de novo lipogenesis. The beneficial effects of Mat1a ASO were abolished following FGF21 depletion in hepatocytes. Thus, targeting Mat1a activates the liver-BAT axis by increasing NRF2-mediated FGF21 secretion, which prevents obesity, insulin resistance and hepatosteatosis., (© 2022. The Author(s).)

Aims: The 5HTT gene has been associated with obesity; this study aimed to determine the association between L- and S-alleles at the 5HTTLPR polymorphism with obesity in indigenous Mexican populations. Materials and Methods: A total of 362 individuals, 289 belonging to eight Native American (NA) groups; 40 Mexican mestizos; and 33 Caucasian Mennonites were enrolled in a cross-sectional study. High (≥90%) and low (<90%) NA ancestry was molecularly determined. A body mass index >30 kg/m 2 was considered as obese. The L- and S-alleles of the 5HTTLPR locus were identified by PCR; the association between alleles and obesity was performed by logistic regression analysis. Results: A significantly lower prevalence of obesity (35%) was observed in participants from communities with high NA ancestry ( p  < 0.005). Under a dominant heritance model the L-allele was associated with obesity in women with high NA ancestry (odds ratio [OR] 7.27; 95% confidence interval [CI] 1.6-32.5; p  = 0.009) but not in women with low NA ancestry (OR 0.83; 95% CI 0.3-2.2; p  = 0.71); no association was observed in men. Conclusion: Our results suggest that the 5HTTLPR L-allele is a risk factor for developing obesity in Mexican women with high NA ancestry (≥90%).

RETRACTED: Obesity is a significant risk factor for acute respiratory distress syndrome. The mechanisms underlying this association are unknown. We recently showed that diet-induced obese mice exhibit pulmonary vascular endothelial dysfunction, which is associated with enhanced susceptibility to LPS-induced acute lung injury. Here, we demonstrate that lung endothelial dysfunction in diet-induced obese mice coincides with increased endoplasmic reticulum (ER) stress. Specifically, we observed enhanced expression of the major sensors of misfolded proteins, including protein kinase R-like ER kinase, inositol-requiring enzyme α, and activating transcription factor 6, in whole lung and in primary lung endothelial cells isolated from diet-induced obese mice. Furthermore, we found that primary lung endothelial cells exposed to serum from obese mice, or to saturated fatty acids that mimic obese serum, resulted in enhanced expression of markers of ER stress and the induction of other biological responses that typify the lung endothelium of diet-induced obese mice, including an increase in expression of endothelial adhesion molecules and a decrease in expression of endothelial cell-cell junctional proteins. Similar changes were observed in lung endothelial cells and in whole-lung tissue after exposure to tunicamycin, a compound that causes ER stress by blocking N-linked glycosylation, indicating that ER stress causes endothelial dysfunction in the lung. Treatment with 4-phenylbutyric acid, a chemical protein chaperone that reduces ER stress, restored vascular endothelial cell expression of adhesion molecules and protected against LPS-induced acute lung injury in diet-induced obese mice. Our work indicates that fatty acids in obese serum induce ER stress in the pulmonary endothelium, leading to pulmonary endothelial cell dysfunction. Our work suggests that reducing protein load in the ER of pulmonary endothelial cells might protect against acute respiratory distress syndrome in obese individuals.

Background: Whether low serum magnesium is an epiphenomenon related with obesity or, whether obesity per se is cause of hypomagnesemia, remains to be clarified., Objective: To examine the relationship between body weight status and hypomagnesemia in apparently healthy subjects., Methods: A total of 681 healthy individuals aged 30 to 65years were enrolled in A cross-sectional study. Extreme exercise, chronic diarrhea, alcohol intake, use of diuretics, smoking, oral magnesium supplementation, diabetes, malnutrition, hypertension, liver disease, thyroid disorders, and renal damage were exclusion criteria. Based in the Body Mass Index (BMI), body weight status was defined as follows: normal weight (BMI <25kg/m 2 ); overweight (BMI ≥25<30 BMIkg/m 2 ); and obesity (BMI ≥30kg/m 2 ). Hypomagnesemia was defined by serum magnesium concentration ≤0.74mmol/L. A multiple logistic regression analysis was used to compute the odds ratio (OR) between body weight status (independent variables) and hypomagnesemia (dependent variable)., Results: The multivariate logistic regression analysis showed that dietary magnesium intake (OR 2.11; 95%CI 1.4-5.7) but no obesity (OR 1.53; 95%CI 0.9-2.5), overweight (OR 1.40; 95%CI 0.8-2.4), and normal weight (OR 0.78; 95%CI 0.6-2.09) were associated with hypomagnesemia. A subsequent logistic regression analysis adjusted by body mass index, waist circumference, total body fat, systolic and diastolic blood pressure, and triglycerides levels showed that hyperglycemia (2.19; 95%CI 1.1-7.0) and dietary magnesium intake (2.21; 95%CI 1.1-8.9) remained associated with hypomagnesemia., Conclusions: Our results show that body weight status is not associated with hypomagnesemia and that, irrespective of obesity, hyperglycemia is cause of hypomagnesemia in non-diabetic individuals., (Copyright © 2016 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)

IL-15Rα is the widely expressed primary binding partner for IL-15. Because of the wide distribution in nonlymphoid tissues like skeletal muscle, adipose, or liver, IL-15/IL-15Rα take part in physiological and metabolic processes not directly related to immunity. In fast muscle, lack of IL-15Rα promotes an oxidative switch, with increased mitochondrial biogenesis and fatigue resistance. These effects are predicted to reproduce some of the benefits of exercise and, therefore, improve energy homeostasis. However, the direct effects of IL-15Rα on metabolism and obesity are currently unknown. We report that mice lacking IL-15Rα (IL-15Rα(-/-)) are resistant to diet-induced obesity (DIO). High-fat diet-fed IL-15Rα(-/-) mice have less body and liver fat accumulation than controls. The leaner phenotype is associated with increased energy expenditure and enhanced fatty acid oxidation by muscle mitochondria. Despite being protected against DIO, IL-15Rα(-/-) are hyperglycemic and insulin-resistant. These findings identify novel roles for IL-15Rα in metabolism and obesity., (Copyright © 2015 the American Physiological Society.)

Obesity is a risk factor for the development of acute respiratory distress syndrome (ARDS) but mechanisms mediating this association are unknown. While obesity is known to impair systemic blood vessel function, and predisposes to systemic vascular diseases, its effects on the pulmonary circulation are largely unknown. We hypothesized that the chronic low grade inflammation of obesity impairs pulmonary vascular homeostasis and primes the lung for acute injury. The lung endothelium from obese mice expressed higher levels of leukocyte adhesion markers and lower levels of cell-cell junctional proteins when compared to lean mice. We tested whether systemic factors are responsible for these alterations in the pulmonary endothelium; treatment of primary lung endothelial cells with obese serum enhanced the expression of adhesion proteins and reduced the expression of endothelial junctional proteins when compared to lean serum. Alterations in pulmonary endothelial cells observed in obese mice were associated with enhanced susceptibility to LPS-induced lung injury. Restoring serum adiponectin levels reversed the effects of obesity on the lung endothelium and attenuated susceptibility to acute injury. Our work indicates that obesity impairs pulmonary vascular homeostasis and enhances susceptibility to acute injury and provides mechanistic insight into the increased prevalence of ARDS in obese humans.

Background: Obesity represents an important health problem and its association with cardiovascular risk factors is well-known. The aim of this work was to assess the correlation between obesity and mortality (both, all-cause mortality and the combined variable of all-cause mortality plus the appearance of a non-fatal first cardiovascular event) in a general population sample from the south-east of Spain., Materials and Methods: This prospective cohort study used stratified and randomized two-stage sampling. Obesity [body mass index (BMI) ≥ 30 kg/m(2)] as a predictive variable of mortality and cardiovascular events was assessed after controlling for age, sex, cardiovascular disease history, high blood pressure, diabetes mellitus, hypercholesterolemia, high-density lipoprotein/triglycerides ratio, total cholesterol and smoking with the Cox regression model., Results: The mean follow-up time of the 1,248 participants was 10.6 years. The incidence of all-cause mortality during this period was 97 deaths for every 10,000 person/years (95% CI: 80-113) and the incidence of all-cause mortality+cardiovascular morbidity was 143 cases for every 10,000 person/years (95% CI: 124-163). A BMI ≥ 35 kg/m(2) yielded a hazard ratio for all-cause mortality of 1.94 (95% CI: 1.11-3.42) in comparison to non-obese subjects (BMI <30 kg/m(2)). For the combination of cardiovascular morbidity plus all-cause mortality, a BMI ≥ 35 kg/m(2) had a hazard ratio of 1.84 (95% CI: 1.15-2.93) compared to non-obese subjects., Conclusions: A BMI ≥ 35 kg/m(2) is an important predictor of both overall mortality and of the combination of cardiovascular morbidity plus all-cause mortality.

Objective: Obesity in children and adolescents is associated to a morbidity that has increased significantly. It has become a public health problem around the world. The objective of this paper was to evaluate the efficacy of the cognitive behavioral treatment strategy in the comprehensive management of obesity in adolescents., Methods: Double blind, randomized, and controlled intervention study, of four months of follow-up, with a total of 115 obese adolescents, aged 12 to 16 years. The intervention group received cognitive behavioral treatment strategy, as well as advise on diet and exercise. At the same time, the control group only received advise on diet and exercise., Results: The percentage of adolescents who showed adherence to diet was 73.7 % versus 41.4 %, (p = 0.0009) and to exercise, 61.4 % versus 19.0 %, (p < 0.0005); compared with the control group, the intervention group was significantly higher. A total of 10 adolescents (17.5 %) in the intervention group and 26 (44.8 %) in the control group dropped-out (p = 0.003). Despite there were significant differences between groups, adolescents in the intervention group exhibited a higher and sustained decrease in body weight, body mass index, as well as in the body fat percentage., Conclusions: The cognitive behavioral treatment strategy improves adherence and decreases desertion of the weight reduction program in adolescents.

Objective: To evaluate the association between Haptoglobin (HP) gene polymorphisms with inflammatory status in obese subjects., Materials and Methods: A cross-sectional study was carried out. A total of 276 apparently healthy men and nonpregnant obese women were enrolled and allocated according to the HP genotype into the HP (1)/HP (1), HP (2)/HP (1), and HP (2)/HP (2) groups. Distribution of HP genotypes was 49, 87, and 140 for the HP (1)/HP (1), HP (2)/HP (1), and HP (2)/HP (2), respectively. The HP genotype was determined using the polymerase chain reaction method. A multiple linear regression analysis adjusted by age, sex, waist circumference, and total body fat was used to determine the association between HP genotypes with TNF- α , IL-6, and high-sensitivity C-reactive protein (hsCRP) levels., Results: A multiple linear regression analysis adjusted by sex, waist circumference, and total body fat was performed showing a significant association between the HP (2)/HP (2) genotype and TNF- α ( β = 0.180; 95% CI 14.41-159.64, P = 0.01) and IL-6 ( β = 0.188; 95% CI 1.53-12.72, P = 0.01) levels, but not with hsCRP ( β = -0.008; 95% CI -1.64-1.47, P = 0.914) levels, whereas the HP (2)/HP (1) genotype showed no association compared with the HP (1)/HP (1) genotype (control group)., Conclusion: Results of our study show that the HP (2)/HP (2) genotype is associated with elevated TNF- α and IL-6, but not with hsCRP, levels in obese subjects.

Background: Given that hypomagnesemia is related with hyperglycemia, hypertension, hypertriglyceridemia, and insulin resistance, the objective of this study was to determine whether serum magnesium levels are associated with the metabolically obese normal weight (MONW) and the metabolically healthy obese (MHO) phenotypes., Methods: Population-based cross-sectional study that enrolled 427 subjects, men and non-pregnant women aged 20 to 65years, to participate in the study. Subjects were allocated into groups with and without obesity; among non-obese individuals, the subgroup of MONW subjects was compared with a control group of healthy normal-weight individuals. Among obese individuals, the subgroup of MHO subjects was compared with a control group of obese subjects who exhibited at least one metabolic abnormality. In the absence of obesity, the presence of fasting hyperglycemia, insulin resistance, hypertriglyceridemia, and/or hypertension defined the presence of MONW phenotype. In the absence of hypertension, insulin resistance and metabolic abnormalities of fasting glucose and triglycerides levels, the phenotypically obese subjects were defined as MHO individuals., Results: The sex-adjusted prevalence of MONW and MHO phenotypes was 40.8% and 27.9%. The multivariate logistic regression model adjusted by family history of diabetes, age, body mass index, and waist-circumference, showed a positive association between hypomagnesemia and the MONW phenotype (OR 6.4; 95%CI 2.3-20.4) and negative relationship between serum magnesium and the MHO phenotype (OR 0.32; 95%CI 0.17-0.61)., Conclusions: Our results show that hypomagnesemia is positively associated with the presence of MONW phenotype, and the normomagnesemia negatively with the MHO phenotype., (Copyright © 2013. Published by Elsevier B.V.)

Objective: To establish the biochemical characteristics of nonobese, overweight, and obese children as well as to determine the risk factors associated with insulin resistance in nonobese children and with non-insulin resistance in obese children in the age strata of 6 to 11 years., Methods: A total of 3512 healthy children were enrolled in a cross-sectional study. In the absence of obesity, fasting hyperinsulinemia and hypertriglyceridemia defined nonobese, insulin-resistant (NO-IR) children. In the absence of metabolic abnormalities of fasting insulin and triglycerides levels, obese children were defined as obese, not insulin-resistant (O-NIR) children., Results: The gender- and age-adjusted prevalence of NO-IR and O-NIR was 6.6% and 21.3%, respectively. In the age-, gender-, and birth weight-adjusted analysis, family history of hypertension (FHH) in both maternal and paternal branches (odds ratio [OR]: 1.514; 95% confidence interval [CI]: 1.2-3.9; P = .04) was associated with NO-IR children. In the analysis adjusted by gender, age, waist circumference (WC), BMI, FHH, and family history of diabetes, high birth weight was associated with NO-IR children (OR: 1.319; 95% CI: 1.2-2.1; P = .04). Finally, in the gender-, age-, family history-, and birth weight-adjusted analysis, a WC lower than the 95th percentile was associated with a lower odds of insulin resistance among obese children (OR: 0.96; 95% CI: 0.91-0.98; P < .0005)., Conclusions: FHH and high birth weight are associated with NO-IR children, and a low WC is associated with lower odds of O-IR children.

We evaluate the relationship between different lipoproteins and atherogenic indices with pre-hypertension in 297 obese and 942 non-obese children with Tanner stage 1 enrolled in a multicentre, community-based cross-sectional study. Height, weight, fasting glucose and insulin levels, total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), non-HDL-c, LDL/HDL-c, triglycerides/cholesterol and total cholesterol/HDL-c ratios were measured. Mean age was 8.4 ± 1.2 years; pre-hypertension was identified in 104 (8.4%) participants, 46 (15.5%) obese and 58 (6.1%) non-obese children. The pre-hypertensive non-obese children show a high proportion of family history of hypertension (41.6 and 24.7%, p = 0.002) and elevation of insulin at a relatively low body mass index. The triglycerides:HDL-c ratio, but not other lipoproteins or atherogenic indices, was associated with pre-hypertension in obese (1.15, 95% confidence intervals 1.06-1.26) and non-obese children (1.38 95% confidence intervals 1.22-1.57). The triglycerides:HDL-c ratio is related to pre-hypertension in children; the family history of hypertension seems to be a risk factor in developing pre-hypertension.

Chronic systemic inflammation, characterized by elevated levels of the acute phase proteins, such as C-reactive protein (CRP), plays an important role in the pathogenesis of glucose metabolic disturbances and diabetes. The aim of this study was to determine if the elevated levels of CRP are associated with impaired fasting glucose (IFG) in obese subjects. Healthy obese men and nonpregnant obese women were enrolled in a case-control study. Individuals with new diagnosis of IFG were considered as cases and compared with a control group without IFG. Elevated CRP was defined by high-sensitivity C-reactive protein (hsCRP) levels between 3.0 and 10.0 mg/L and new diagnosis of IFG by the presence of fasting plasma glucose levels of 100 to 126 mg/dL. A total of 74 subjects were allocated into the case group and compared with 74 subjects in the control group. Elevated hsCRP was identified in 61 (41.2 %) and 34 (23.0 %) individuals in the case and control groups, respectively (p < 0.001). The adjusted odds ratio used to assess the association between elevated hsCRP levels and IFG was 3.36; 95 % confidence interval was 1.66-6.79. In conclusion, the elevated hsCRP levels are associated with IFG in obese subjects.

Objective: To evaluate the efficacy of low carbohydrate diet (LCD) as compared with low fat diet (LFD) to decrease aminotransferase levels in obese women with nonalcoholic fatty liver disease., Material and Methods: A total of 59 women were randomly enrolled in a non-controlled clinical intervention study to receive either LCD or LFD during six months. Apparently healthy non-pregnant obese women aged 20 to 65 years were eligible to participate. Previous diagnosis of hepatic disease, serum creatinine level ≥ 1.5 mg/dL, severe life-limiting medical illness, pregnancy, active participation in other dietary program, use of weight loss drugs, or alcohol consumption ≥ 30 g per day were exclusion criteria., Results: A total of 31 obese women who received LCD were compared with 28 women allocated in the LFD group. There were 3 (LCD group) and 2 (LFD group) women with lost of follow-up. No differences in the proportion of type 2 diabetes, hypertension and hyperlipidemia were noted between women in the LCD and LFD groups. At end of follow-up, there were not significant statistical differences in the anthropometric and biochemical characteristics between women in both groups. The weight loss was 5.7 and 5.5% for women in the LCD LFD groups. Although the decrease of AST (31.7 and 22.4%) and ALT (41 and 33.3%) levels was more elevated in the women of LCD group, as compared with the LFD group, there were not significant statistical differences., Conclusions: Our results show that weight loss, irrespective of the type of diet, reduces aminotransferase levels in obese women with NAFLD.

Objective: To determine whether the association between family history of diabetes (FHD) and impaired fasting glucose (IFG) is independent of body mass index (BMI) in children and adolescents., Methods: In all 443 (11.9%) children and adolescents with FHD, and 3280 (88.1%) without FHD were enrolled in a population-based cross-sectional study. Eligible subjects to participate were apparently healthy children and adolescents aged 7-15 yr from Middle and Northern Mexico. Obesity was defined by age- and gender-specific BMI >or= 95th percentile. FHD was defined as positive if at least one first degree relative had diabetes. The IFG was defined by fasting plasma glucose >or= 100 mg/dL and < 126 mg/dL., Results: IFG was identified in 390 (88.0%) and 62 (1.9%) children and adolescents with and without FHD, respectively. In the group with positive FHD, IFG was diagnosed in 146 (37.4%), 79 (20.2%), and 165 (42.3%) children and adolescents who were obese, overweight, and normal-weight, respectively. On the other hand, in the group without FHD, IFG was identified in 21 (33.9%), 14 (22.6%), and 27 (43.5%) children and adolescents who were obese, overweight, and normal-weight, respectively. In the overall population, the age-, sex-, and BMI-adjusted logistic regression analysis showed a strong and independent association between FHD and IFG [odds ratio (OR) -11.7; 95% CI 9.5-21.2]. This association remained strong for girls and boys in a subsequent analysis stratified for BMI category., Conclusions: The presence of FHD in a first degree relative is associated with IFG, even in the absence of obesity.

To evaluate the effect of oral supplementation with magnesium chloride on the systemic and hepatic inflammation, 38 non-hypertensive obese women aged 30 to 65 years were allocated into groups with and without hypomagnesemia. Hypomagnesemic women drank 50 mL of 5% solution of MgCl2 equivalent to 450 mg of elemental magnesium. Low-carbohydrate diets and physical activity were indicated for women in both groups. Chronic diarrhea, alcohol intake, use of diuretics, previous oral magnesium supplementation, hepatic disease, and renal damage were exclusion criteria. Hypomagnesemia is defined by serum magnesium concentrationsor=40 U/L, and systemic inflammation by serum high-sensitivity C reactive protein (hs-CRP) concentration>or=3 mg/L. At baseline (p=0.06) and final of follow-up (p=0.80), there were no significant differences by body mass index between the groups in the study. In the same way, at baseline ALT (48.1+/-25.5 and 34.6+/-24.1 U/L, p=0.14) and hs-CRP (9.4+/-6.0 and 7.9+/-5.9 mg/dL, p=0.47) levels were similar in the supplemented and non-supplemented women. In the magnesium group, ALT (24.3+/-10.3 and 34.8+/-13.6 U/L, p=0.02) levels, but not hs-CRP (5.2+/-1.9 and 8.0+/-5.6 mg/L, p=0.08) reached significantly lower levels, in the fourth month of treatment, than in women in the control group. The adjusted odds ratios between the improvement in serum magnesium and reduction in ALT and hs-CRP levels were 0.56 (95% CI: 0.3-0.9) and 0.93 (95% CI: 0.6-29.9), respectively. Results of this study show that in hypomagnesemic obese women, oral supplementation with magnesium chloride reduces plasma ALT levels; hs-CRP levels only show a reduction trend.

Objective: To determine the clinical characteristics of NAFLD in asymptomatic obese women., Methods: A total of 457 asymptomatic obese women were enrolled in a cross-sectional study and allocated into groups with and without NAFLD. Irrespective of ALT levels, diagnosis of NAFLD was established by ultrasonographic findings; irrespective of fibrosis, NASH was defined by hepatic histological changes., Results: One hundred ninety five (42.7%) women had elevated ALT levels. Diagnosis of NAFLD was established in 228 (49.9%) women; among women with NAFLD, 34 (14.9%) have ALT levels within the normal range. On the other hand, based on the healthy range for ALT levels (19 UI/L), 336 (73.5%) women had elevated ALT, but only 2 (0.9%) women with NAFLD exhibited ALT levels within normal healthy values. Furthermore, 93 (41%) women who had AST/ALT levels (3) 1 underwent liver biopsy; of these, 90 (96.8%) had diagnosis of NASH and 3 (3.2%) of hepatic cirrhosis. Women with NAFLD were more obese and have higher fasting plasma glucose, triglycerides, ALT, and AST levels than obese women without NAFLD. Seventy six (16.6%) women had diagnosis of diabetes; of these 47 (61.8) in the NAFLD group., Conclusions: Results of this study support the statement that women with NAFLD have an adverse metabolic profile. Furthermore, our results show that hyperglycemia, hypertriglyceridemia and markers of liver injury such as AST/ALT > or = 1 may be useful for early recognition of NAFLD.

To evaluate the efficacy of adding cognitive behavioural treatment (CBT) to either a low-carbohydrate (LC) diet or a low-fat (LF) diet in the treatment of weight loss of obese women, a randomised clinical intervention study was performed. A total of 105 healthy non-pregnant obese women (average age and BMI of 45.4 (sd 10.4) years and 36 (sd 4.3) kg/m2) were randomly allocated to the CBT or control (C) groups; within each group, women were randomly selected to receive either the LC or LF diet during 6 months. The pre-planned primary trial end-point was the weight loss. Differences between the groups were assessed using one-way ANOVA. There were three women (2.8 %) who dropped out, all of them in the CBT group. No differences in the anthropometric and laboratory characteristics at baseline were noted between women in the CBT (n 52) and control groups (n 50). Intention-to-treat analysis showed that weight loss in the CBT-LC (90 (sd 12.3) to 82.1 (sd 12.1) kg) and C-LC (89.4 (sd 10.0) to 85.8 (sd 9.8) kg) groups reached 8.7 and 4.0 %, respectively (P < 0.0001), and in the CBT-LF (87.9 (sd 11.4) to 79.4 (sd 11.8) kg) and C-LF (88.8 (sd 14.5) to 85.3 (sd 14.3) kg) groups it was 9.7 and 3.9 %, respectively (P < 0.05). Weight loss was higher in the CBT-LF group than in the CBT-LC groups (P = 0.049). The present results showed that adding CBT to either the LF or LC diet produced significantly greater short-term weight loss in obese women compared with diet alone. These finding support the efficacy of CBT in breaking previous dietary patterns and in developing healthier attitudes that reinforce a healthier lifestyle.

Obesity-induced chronic inflammation leads to activation of the immune system that causes alterations of iron homeostasis including hypoferraemia, iron-restricted erythropoiesis, and finally mild-to-moderate anaemia. Thus, preoperative anaemia and iron deficiency are common among obese patients scheduled for bariatric surgery (BS). Assessment of patients should include a complete haematological and biochemical laboratory work-up, including measurement of iron stores, vitamin B12 and folate. In addition, gastrointestinal evaluation is recommended for most patients with iron-deficiency anaemia. On the other hand, BS is a long-lasting inflammatory stimulus in itself and entails a reduction of the gastric capacity and/or exclusion from the gastrointestinal tract which impair nutrients absorption, including dietary iron. Chronic gastrointestinal blood loss and iron-losingenteropathy may also contribute to iron deficiency after BS. Perioperative anaemia has been linked to increased postoperative morbidity and mortality and decreased quality of life after major surgery, whereas treatment of perioperative anaemia, and even haematinic deficiency without anaemia, has been shown to improve patient outcomes and quality of life. However, long-term follow-up data in regard to prevalence, severity, and causes of anaemia after BS are mostly absent. Iron supplements should be administered to patients after BS, but compliance with oral iron is no good. In addition, once iron deficiency has developed, it may prove refractory to oral treatment. In these situations, IV iron (which can circumvent the iron blockade at enterocytes and macrophages) has emerged as a safe and effective alternative for perioperative anaemia management. Monitoring should continue indefinitely even after the initial iron repletion and anaemia resolution, and maintenance IV iron treatment should be provided as required. New IV preparations, such ferric carboxymaltose, are safe, easy to use and up to 1000 mg can be given in a single session, thus providing an excellent tool to avoid or treat iron deficiency in this patient population.

Published data on the distribution of fasting plasma glucose (FPG) in children are scarce. We therefore set out to examine the distribution of FPG and determine the prevalence of impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and type 2 diabetes (T2-DM) in Mexican children aged 6-18 years in a community-based cross-sectional study. A total of 1534 apparently healthy children were randomly enrolled and underwent an oral glucose tolerance test. IFG was defined by an FPG value between >or=100 and <126 mg/dL, IGT by glucose concentration 2-h post-load between >or=140 and <200 mg/dL, and T2-DM by glucose concentration 2-h post-load >or=200 mg/dL. The FPG level at the 75(th) percentile of distribution was 98.0, 100.0 and 99.0 mg/dL for children aged 6-9, 10-14 and 15-18 years, respectively; the 95(th) percentile of FPG was greater than 100 mg/dL for all the age strata. In the population overall, the prevalences of IFG, IGT, and T2-DM were 18.3%, 5.2% and 0.6%, respectively. Among obese children and adolescents, the prevalences of IFG, IGT, IFG + IGT and T2-DM were 19.1%, 5.7%, 2.5% and 1.3%. Our study shows a high prevalence of prediabetes and is the first that reports the distribution of FPG in Mexican children and adolescents.

Objective: To assess the hypothesis that magnesium deficiency is associated with elevated high-sensitivity C-reactive protein (hsCRP) levels., Design: Community-based cross-sectional study., Setting: 488 apparently healthy children aged 10-13 years were randomly enrolled from Durango, a city in northern Mexico, through two-stage cluster sampling., Main Outcome Measures: Serum magnesium and hsCRP levels, lipid profile, glucose and insulin levels., Results: A total of 109 (22.3%) and 101 (20.7%) children had elevated hsCRP concentrations and low serum magnesium levels; among them, 87.1% exhibited both. Children who had both elevated hsCRP levels (2.45 (10.6) mg/l) and hypomagnesemia (1.3 (0.3) mg/dl) exhibit the highest fasting glucose (96.0 (13.9) mg/dl), insulin (13.6 (7.5) microU/ml) and triglycerides (131.5 (43.5) mg/dl) levels as well as the lowest HDL-cholesterol (46.4 (9.0) mg/dl) levels. Adjusted multivariate logistic regression analysis showed a strong association between low serum magnesium and high hsCRP levels (odds ratio 4.1; 95% confidence interval 1.3 to 10.8)., Conclusions: Magnesium depletion is independently associated with elevated hsCRP levels, suggesting that hypomagnesemia and low-grade inflammation are interactive risk factors.

Objective: to determine the relationship between the abdominal obesity and cardiovascular risk factors in apparently healthy subjects from Mexico City., Methods: a total of 186 apparently healthy men and nonpregnant women from Mexico City, were enrolled in a cross-sectional study. A detailed medical history and physical examination were performed. Abdominal obesity was defined by waist circumference > or = 80 cm for women and > or = 90 cm for men., Results: a total of 125 women (67.2 %) and 61 men (32.8 %) were enrolled. Of them, 151 (81.2 %) had insulin resistance and 130 (69.9 %) abdominal obesity. Among obese subjects 96 (46.2 %) showed metabolic syndrome. There were a high prevalence of hypertriglyceridemia (31 %) and low serum levels of HDL-cholesterol (58 %)., Conclusions: the used cut point for abdominal obesity, despite identifying a high proportion of subjects with cardiovascular risk, did not recognize a high proportion of subjects with disorders in their lipid profile.

Objective: The objective of this study is to determine the association between risk factors and nonalcoholic fatty liver disease (NAFLD), and to establish the relationship between risk factors and hepatic histological changes in obese women., Methods: A case-control design study. Women with NAFLD (cases) were compared with a control group of obese women without NAFLD matched by age, body mass index, waist circumference, and body fat. Irrespective of serum aminotransferases levels, diagnosis of NAFLD was established by the presence of type II diabetes, hypertriglyceridemia, and ultrasonographic changes of hepatic steatosis. Diagnosis of nonalcoholic steatohepatitis was performed by a liver biopsy. Women with an aspartate aminotransferase/alanine aminotransferase (ALT) ratio of at least 1 underwent liver biopsy. Alcohol consumption, hepatitis, and drugs that promote cholestasis or liver injury were the exclusion criteria. Multiple regression analysis was used to compute the association between the risk factors and NAFLD, and Spearman's analysis was used to examine its relationship with histological hepatic changes., Results: A total of 108 obese women were enrolled. The frequency of high blood pressure, hypertriglyceridemia, and diabetes was similar between the groups. ALT (54.4+/-33.3 and 39.8+/-29.8, P=0.03) but not aspartate aminotransferase (45.4+/-23.1 and 36.7+/-21.2, P=0.06) was significantly higher in the women with NAFLD. The multivariate regression analysis showed a significant association of ALT (odds ratio 2.7; 95% confidence interval, 1.3-10.4), but not other variables with NAFLD. Type II diabetes was strongly correlated with ballooning and inflammation, and ALT with inflammation and fibrosis., Conclusion: Obese women with similar metabolic alterations exhibit different hepatic outcomes. Elevation of ALT, but not other risk factors, was associated with NAFLD. Diabetes and ALT correlate with histological hepatic changes.

Background: Epidemiological data on impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) based on a representative Mexican sample are not available; thus, the objectives of this study were to determine the prevalence and distribution of IFG and IGT, and to establish its relationship with obesity in Mexican adults., Methods: We performed a cross-sectional population-based study on a representative sample of Mexican adults aged 30 to 65 years. Anthropometric measurements of obesity that included waist circumference (WC) and total body fat percentage were collected and the body mass index calculated. All subjects also underwent an oral glucose tolerance test. Diagnosis of glucose metabolism disorders was based on criteria of the American Diabetes Association., Results: Prevalence of IFG, IGT, and IFG+IGT was 24.6%, 8.3%, and 10.3%, respectively. The age-adjusted prevalence of IFG (49.5% and 50.5%), IGT (49.1% and 50.9%), and IFG+IGT (57.3% and 42.7%) was similar in men and women. Prevalence of obesity was 45.9% with predominance in women (48.8% versus 42.1%, P = 0.01). A total of 394 (31.0%) individuals were overweight. Among the 550 prediabetic normal weight subjects, 70 (22.4%), 15 (14.2%), and 7 (5.3%) had IFG, IGT, or IFG+IGT. The odds ratio (OR) between WC and IFG (OR 3.1, CI(95%) 1.4-9.7), IGT (OR 3.2, CI(95%) 1.2-9.1), and IFG+IGT (OR 2.8, CI(95%) 1.3-8.2) was higher than the OR of other measurements of obesity., Conclusions: Prevalence of prediabetes in the Mexican adult population is high. WC is the measure of obesity more strongly associated with metabolic glucose disorders. A high proportion of subjects with normal weight exhibit prediabetes.

Background: Some lines of evidence suggest that endotoxin may induce non-alcoholic steatohepatitis (NASH) in a background of fatty liver. However, a clear association between increased endotoxemia and development of steatohepatitis in obese patients has not been confirmed. We aim to assess the endotoxemic state of patients with non-alcoholic fatty liver disease (NAFLD) and its relationship with the liver expression of TNF-alpha and the presence of NASH., Methods: Prospective study comprising 40 patients with morbid obesity who were diagnosed with NAFLD. Blood samples and liver biopsies were collected. Endotoxemia was assessed by the evaluation of circulating level of LPS-binding protein (LBP). Plasma levels of LBP and TNF-alpha were assessed by ELISA. The expression of TNF-alpha in liver tissue was evaluated by real-time PCR. Histological examination was performed to evaluate the presence of steatosis or NASH., Results: Levels of LBP were increased in obese patients with NAFLD. In addition, plasma level of LBP was increased in patients with steatohepatitis (14.2 +/- 3.9 microg/mL) when compared with patients with simple steatosis (11.5 +/- 3.2 microg/mL), P=0.041. The TNF-alpha mRNA expression in liver tissue was significantly higher in patients with NASH. This increment correlated with the rise in plasma levels of LBP (r=0.412, P=0.036)., Conclusion: NAFLD patients have elevated plasma levels of LBP and they are further increased in patients with NASH. This increase is related to a rise in TNF-alpha gene expression in the hepatic tissue which supports a role for endotoxemia in the development of steatohepatitis in obese patients.

Background: Because obesity masks the need for screening, there is no previous description of dyslipidemia in healthy normal-weight children. The aims of this study were a) to determine the prevalence of disorders in lipid profile among non-obese prepubertal children, and b) to establish its association with the family history (FH) of high blood pressure (HBP), type 2 diabetes (T2-DM), and obesity., Methods: A random sample of 439 healthy normal-weight children, 218 girls and 221 boys, aged 10-13 years and Tanner stage 1-2 were enrolled in a community-based cross-sectional study carried out in Durango, in northern Mexico. For verifying accuracy of FH, a direct detailed medical history including anthropometric and laboratory measurements was directly obtained from both parents., Results: Among parents, prevalence (95% CI) of T2-DM, HBP, and obesity was 8.3% (3.5-14.3), 14.2% (8.6-24.6), and 28.5% (24-33), and for hypercholesterolemia, low HDL-cholesterol, high LDL-cholesterol, hypertriglyceridemia, and mixed hyperlipidemia 17.9 % (15-20), 27.8% (25-30), 14.3% (12-16), 32.3% (29-35), and 9.8 % (8-12), respectively. Among children, prevalence (95% CI) for high total cholesterol, low HDL-cholesterol, high LDL-cholesterol, isolated hypertriglyceridemia, and mixed hyperlipidemia was 15.9% (12.6-19.5); 6.2% (4.0-8.5); 14.6% (11.4-18.0); 9.3% (6.7-12.2); and 3.6% (2.1-5.8), respectively. Sex- and birth weight-adjusted odds ratio (95% CI) showed that FH of T2-DM, but not of HBP and obesity, was associated with hypercholesterolemia (2.1; 1.2-6.2), low HDL-cholesterol (1.8; 1.1-5.7), and hypertriglyceridemia (2.3; 1.1-6.4)., Conclusions: Non-obese children in this sample display a high prevalence of abnormalities in lipid profile associated with FH of T2-DM.

Background: Epidemiological evidence shows a strong relationship between decreased serum magnesium levels (DSML) and insulin resistance. As nonalcoholic steatohepatitis (NASH) seems to be related to insulin resistance, the aim of this study was to determine the potential relationship between DSML and NASH in obese subjects., Methods: We compared obese individuals with the diagnosis of diabetes, insulin-resistance, and non-insulin resistance to a control group of non-obese, non-insulin-resistant subjects. Participants were required to have negative viral markers and negligible alcohol intake. Other liver diseases and well-known causes for decreasing of magnesium were exclusion criteria. A liver biopsy was performed in subjects with aspartate aminotransferase (AST) and alanine aminotransferease (ALT) levels > or =40 IU/mL., Results: Of the 60 obese subjects, 20 were non-insulin resistant, 20 were insulin resistant, and 20 were type 2 diabetics. Twenty subjects were in the control group. Eleven (33.3%) diabetics, 14 (42.4%) insulin-resistant subjects, and 8 (24.2%) non-insulin-resistant subjects underwent liver biopsies. Diagnosis of NASH was established in 29 (36.2%) individuals. Subjects with the diagnosis of NASH exhibited lower serum magnesium levels of 1.7 +/- 0.2 mg/dL (0.70 +/- 0.08 mmol/L), and those with fibrosis showed the lowest serum magnesium concentration at 1.5 +/- 0.3 mg/dL (0.62 +/- 0.12 mmol/L). Multiple regression analysis adjusted by age showed that low serum magnesium concentration was independently related to a high HOMA-IR index (OR 7.6, CI 95% 2.1-11.2; p <0.0001) and that a high HOMA-IR index was related to NASH (OR 6.5, CI 95% 1.5-8.8; p <0.01). After adjusting for age and a high HOMA-IR index, hypomagnesemia remained independently related to NASH (OR 1.4, CI 95% 1.1-5.4; p <0.05)., Conclusions: The results of this study demonstrate an independent relationship between DSML and NASH.

The aim of this study was to determine the relationship between serum magnesium and TNF-alpha levels in obese subjects. A cross-sectional population based study that included 192 non-diabetic, non-hypertensive subjects allocated in three categories of body mass index (BMI) <25; > or =25 to <30 kg/m2; and > or =30 kg/m2. Elevation of TNF-alpha levels was defined by serum levels > or =3.5 pg/mL, and low serum magnesium by levels < or = 0.74 mmol/L. Multivariate odds ratios (OR) adjusted by age, HOMA-IR index, and glucose tolerance status are presented. Obese subjects exhibited higher serum concentration of TNF-alpha (p = 0.002) and lower serum magnesium levels (p < 0.0001) than lean and overweight subjects. Ninety-one (47.4%) subjects showed elevated levels of TNF-alpha, of them 7 (10.9%), 31 (48.4%), and 43 (67.2%) in the groups with BMI <25, > or = 25 to < 0, and >> or =0 kg/m2, respectively. Multivariate OR between low serum magnesium and TNF-alpha levels in obese subjects was of 1.8, Cl95% 1.2-9.1, P = 0.001, whereas in the lean and overweight individuals of 1.1, Cl95% 0.7-8.7, P = 0.12, and 1.3, Cl95% 0.9-10.8, P = 0.09, respectively. These data shows that low serum magnesium levels and elevated TNF-alpha are related in the obese subjects. It will be necessary to conduct more studies in order to add new data on this issue.

Background: Our objective was to develop an anthropometric-based index (abdominal volume index, AVI) for estimating overall abdominal volume and to determine its relationship with presence of impaired glucose tolerance (IGT) and type 2 diabetes mellitus (DM)., Methods: We conducted a cross-sectional, population-based study between November 1998 and June 2001 among 746 men and non-pregnant women randomly recruited from Durango City in northern Mexico. AVI was calculated using volume formulas for cylinder (V=pir2h) and vertical cone V=(1/3)pir2h. The formula developed was AVI=[2 cm (waist)2+0.7 cm (waist-hip)2]/1,000, which estimates overall abdominal volume between symphysis of pubis and xiphoid appendix and theoretically includes intra-abdominal fat and adipose tissue volumes., Results: Receiver operating curve (ROC) scatter plot showed as best cut-off value of AVI for estimation of obesity, corresponding to 24.5 liters (L). Logistic regression analysis adjusted by age and sex showed higher odds ratio between AVI and IGT 1.6 (95% confidence interval [95% CI] 1.1-9.1, p=0.01) as well as between AVI and DM 2.1 (95% CI 1.3-7.9, p=0.001) than odds ratio (OR) estimated by other anthropometric obesity criteria such as waist-to-hip ratio, body mass index, truncated cone, and waist circumference., Conclusions: AVI is a reliable and easy-to-calculate anthropometric tool for estimation of overall abdominal volume that is shown to be strongly related to IGT and DM.

Objective: To examine the association between serum magnesium levels and C-reactive protein (CRP) in non-diabetic, non-hypertensive obese subjects., Design: Cross-sectional study., Subjects: A total of 371 subjects, 101 men and 270 women. Of them 138 lean (37.2%), 133 (35.9%) overweight, and 100 (26.9%) were obese, matched by age., Measurements: Fasting and 2 h serum glucose following a 75 g oral glucose load. Fasting serum total cholesterol, HDL- and LDL-cholesterol, triglycerides, C-reactive protein (CRP), albumin; and magnesium levels; urinary protein excretion; body mass index (BMI), waist-to-hip ratio (WHR), and blood pressure., Results: The presence of CRP was documented in four (2.9%) lean, 13 (9.8%) overweight, and 20 (20.0%) obese subjects, and decreased magnesium levels (equal or less than 1.8 mg/dl), in 2 (1.45%) lean, 7 (5.2%) overweight, and 19 (19%) obese subjects. The lowest serum magnesium levels and the highest CRP concentrations were documented in the obese subjects. Twenty-three (82.1%) of the subjects with low serum magnesium (five overweight and 18 obese) showed CRP concentration equal or more than 10 mg/l. There was a graded significant decrease between CRP concentration and serum magnesium levels (r = -0.39, P = 0.002). The odds ratio (CI95%) between magnesium and CRP adjusted by age, sex, BMI and glucose tolerance status for the subjects within the low quartile of magnesium distribution was 2.11 (1.23-3.84)., Conclusion: The results of this study show that low serum magnesium levels are independently related to elevated CRP concentration, in non-diabetic, non-hypertensive obese subjects.

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.

The main aim of this study was to examine the relationship of the leptin system in steatosis and nonalcoholic steatohepatitis (NASH). The study also analysed the pathogenic role of the leptin system in the development of hepatic fibrosis and its relation with the TGF-β1 system. Materials and methods: The study included 90 subjects, 55 with NASH and 35 with simple steatosis. Gene expression of leptin, leptin receptor and TGF-β mRNA was analysed by real-time PCR on liver tissue. Leptin serum levels were determined by RIA. Leptin receptor expression was also assessed by immunohistochemistry. Results: Increased expression was found for leptin receptor mRNA ( P=0.0016) and its protein ( P<0.05) in patients with NASH, especially those with fibrosis. There was a marked increase in gene expression of TGF-β1 in patients with NASH ( P=0.0002). A strong correlation was demonstrated between leptin receptor gene expression and TGF-β1 gene expression ( P=0.023). No leptin expression was found in the liver tissue. All patients showed a marked hyperleptinemia, which was closely related to the anthropometric characteristics analysed and independent of development or not of NASH. Conclusions: The results of the study demonstrate for the first time increased leptin receptor expression in liver tissue and its relationship with overexpression of TGF-β1 and the degree of hepatic fibrosis. [ABSTRACT FROM AUTHOR]

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Examines the association between serum magnesium levels and C-reactive protein in non-diabetic, non-hypertensive obese subjects. Patient characteristics; Link of hypomagnesemia and inflammatory response to the development of glucose metabolic disorders; Inverse correlation of serum magnesium and body mass index.