Polymorphism of neuropeptide Y gene rs16147 modifies the response to a hypocaloric diet on cardiovascular risk biomarkers and adipokines.

BACKGROUND: The main genetic variant described in NPY gene is rs16147 (G-399A) and it is located within the promoter region upstream of the gene for neropeptide Y (NPY). We evaluate the effects of the rs16147 NPY gene polymorphism on metabolic changes secondary to weight loss after 3 months of a hypocaloric diet in adult obese patients. METHODS: A population of 82 obese patients was analysed in an interventional design of one arm. Before and after 3 months on a hypocaloric diet, an anthropometric evaluation, an assessment of nutritional intake and a biochemical analysis were performed. The statistical analysis was performed for combined GA and AA as a group (minor allele group) and GG as second group (major allele group) (dominant model). RESULTS: In A allele carriers, the mean (SD) decrease in weight was -2.8 (2.2) kg [decrease in non A allele carriers -2.6 (1.1) kg, P > 0.05), body mass index was -1.2 (0.6) kg m-2 [decrease in non A allele carriers -1.1 (0.8) kg m-2 , P > 0.05], fat mass was -1.7 (1.4) kg [decrease in non A allele carriers -1.9 (1.3) kg, P > 0.05], waist circumference was -5.5 (3.4) cm [decrease in non A allele carriers -3.7 (4.1) cm, P = 0.006], C-reactive protein (CRP) was -0.7 (0.6) mg dL-1 [decrease in non A allele carriers -0.1 (0.3) mg dL-1 , P = 0.02], insulin was -1.5 (0.4) mUI L-1 [decrease in non A allele carriers -0.8 (2.0) mUI L-1 , P = 0.001] and homeostasis model assessment-insulin resistance (HOMA-IR) was -0.4 (0.5) [decrease in non A allele carriers -0.2 (0.1), P = 0.005]. interleukin (IL)-6 changes were significant in A allele carriers [-0.7 (0.2) pg mL-1 ] versus non A allele carriers [-0.1 (0.3) pg mL-1 ] (P = 0.01). CONCLUSIONS: We found that the rs164147 genotype affected the reduction of waist circumference, HOMA-IR, insulin, CRP and IL-6 levels in response to weight loss diet in obese subjects.

Association of G1359A polymorphism of the cannabinoid receptor gene (CNR1) with macronutrient intakes in obese females.

BACKGROUND: The endogenous cannabinoid system plays a role in metabolic aspects of body weight and feeding behaviour. A polymorphism (1359 G/A) (rs1049353) of the CB1 gene was reported as a common polymorphism in the Caucasian population. The present study aimed to investigate the association of the polymorphism (G1359A) of the CB1 receptor gene on macronutrient intake in females with obesity. METHODS: A sample of 896 females was analysed. A bioimpedance measurement, a blood pressure measurement, a serial assessment of nutritional intake with 3 days of written food records, and a biochemical analysis were all performed. The genotype of the CNR1 receptor gene polymorphism (rs1049353) was studied. RESULTS: Five hundred and sixteen patients (57.6%) had the genotype G1359G (non-A carriers) and 380 (42.4%) patients had G1359A (328 patients, 36.6%) or A1359A (52 patients, 5.8%) (A carriers). Triglycerides and high-density lipoprotein (HDL) cholesterol levels were higher in A non-A allele carriers than non-A allele carriers. The intakes of dietary cholesterol and saturated fat for the upper tertile (T3) compared to the baseline tertile were inversely associated with the CB1-R 1359 G/A polymorphism [odds ratio (OR) = 0.59; 95% confidence interval (CI) = 0.30-0.92 and OR = 0.66; 95% CI = 0.39-0.91, respectively]. These data were observed in the second tertile (T2) (OR = 0.61; 95% CI = 0.29-0.94 and OR = 0.58; 95% CI = 0.31-0.90, respectively). CONCLUSIONS: The present study reports an association of the A allele with a better lipid profile (triglycerides and HDL cholesterol) than non-A allele carriers. In addition, this polymorphism is associated with a specific macronutrient intake, as well as with low cholesterol and fat saturated intakes.

Role of rs6923761 gene variant in glucagon-like peptide 1 receptor in basal GLP-1 levels, cardiovascular risk factor and serum adipokine levels in naïve type 2 diabetic patients.

BACKGROUND: Role of GLP-1 variants on basal GLP-1 levels, body weight and cardiovascular risk factors remains unclear in patients with diabetes mellitus type 2. OBJECTIVE: Our aim was to analyze the effects of rs6923761 GLP-1 receptor polymorphism on body weight, cardiovascular risk factors, basal GLP-1 levels and serum adipokine levels in naïve patients with diabetes mellitus type 2. DESIGN: A sample of 104 naïve patients with diabetes mellitus type 2 was enrolled in a prospective way. Basal fasting glucose, c-reactive protein (CRP), insulin, insulin resistance (HOMA), total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides concentration, basal GLP-1, HbA1c and adipokines (leptin, adiponectin, resistin) levels were determined. Weights, body mass index, waist circumference, fat mass by bioimpedance and blood pressure measures were measured. RESULTS: Forty-nine patients (47.1%) had the genotype GG and 55 (52.9%) diabetic subjects had the next genotypes; GA (44 patients, 42.3%) or AA (11 study subjects, 10.6%) (second group). In A allele carriers, basal GLP-1 levels were higher than non-carriers (2.9 ± 2.1 ng/ml; p < 0.05). No differences were detected between both genotype groups. CONCLUSION: Our cross-sectional study revealed an association between the rs6923761 GLP-1 receptor polymorphism (A allele carriers) and basal GLP-1 levels in naïve patients with diabetes mellitus type 2.

Effects of a high-protein/low-carbohydrate versus a standard hypocaloric diet on adipocytokine levels and cardiovascular risk factors during 9 months, role of rs6923761 gene variant of glucagon-like peptide 1 receptor.

BACKGROUND: The role of GLP-1 R variants on body weight response after dietary intervention is unclear. OBJECTIVE: The aim was to investigate the role of this polymorphism on cardiovascular risk factors, adipokine levels and weight loss secondary to a high-protein/low-carbohydrate vs. standard hypocaloric diets during 9 months. DESIGN: 211 obese subjects were randomly allocated to one of these two diets for a period of 9 months; diet HP (high protein/low carbohydrate) and diet S (standard). RESULTS: Ninety-four patients (44.5%) had the genotype GG (wild group) and 117 (55.5%) patients had the next genotypes; GA (89 patients, 42.2%) or AA (28 patients, 13.3%) (mutant group). With both diets and in both genotype groups, body mass index, weight, fat mass, waist circumference and systolic blood pressure decreased. Anthropometric parameters were higher in non-A allele carriers than A allele carriers. With diet HP in both genotypes, LDL cholesterol, total cholesterol, leptin, insulin levels and HOMA-R decreased. With the diet S and only in wild genotype, the same parameters decreased, too. CONCLUSION: Our data showed a lack of association of rs6923761 GLP-1 R polymorphism with weight loss. Better anthropometric parameters in obese subjects with the mutant allele (A) of rs6923761 GLP-1 R polymorphism were observed. Total cholesterol, LDL cholesterol, insulin levels and HOMA-R decreased in all patients with both diets, although A allele carriers treated with standard diet did not show these changes.

Effect of Lys656Asn Polymorphism of Leptin Receptor Gene on Cardiovascular Risk Factors and Serum Adipokine Levels after a High Polyunsaturated Fat Diet in Obese Patients.

BACKGROUND: Human obesity is characterized by high levels of leptin, and leptin levels may change with weight loss and dietary restriction. The aim of our study was to investigate the influence of Lys656Asn polymorphism in the leptin receptor gene on cardiovascular risk factors, weight loss, and serum leptin levels to a high polyunsaturated fatty acid (PUFA) hypocaloric diet in obese patients. DESIGN: A sample of 132 obese patients was analyzed in a prospective way with a dietary intervention. The enriched PUFAs hypocaloric intervention consisted in a diet of 1,459 kcal, 45.7% of carbohydrates, 34.4% of lipids, and 19.9% of proteins. RESULTS: In wild-type group, BMI (-1.9 ± 1.4 kg/m(2) ), weight (-4.4 ± 3.2 kg), fat mass (-4.2 ± 3.8 kg), waist circumference (-4.1 ± 3.1 cm), systolic blood pressure (-7.0 ± 12.1 mmHg), diastolic blood pressure (-3.9 ± 6.8 mmHg), insulin (-1.8 ± 5.6 MUI/l) and HOMA-IR (-0.5 ± 1.5 Units) decreased. In mutant genotype group, BMI (-2.0 ± 2.1 kg/m(2) ), weight (-3.6 ± 4.1 kg), waist circumference (-3.1 ± 4.1 cm), total cholesterol (-25.2 ± 19.6 mg/dl), LDL cholesterol (-16.6 ± 25.6 mg/dl), and tryglicerides (-26.6 ± 39.1 mg/dl) decreased. Only leptin levels have a significant decrease in wild genotype group (-6.6 ± 10.2 ng/ml) (25.1%). CONCLUSION: Carriers of ASn656 allele have a different response than wild-type obese, with a lack of decrease in insulin levels, leptin levels, and HOMA-IR. However, obese patients with this mutant allele have a better lipid profile after weight loss.

Serum visfatin levels and metabolic syndrome criteria in obese female subjects.

BACKGROUND: Serum visfatin concentrations are associated with cardiovascular risk factors and obesity. Relation of this adipokine with metabolic syndrome is unclear. We decide to investigate the association between metabolic syndrome and visfatin levels in female obese subjects. SUBJECTS: A sample of 826 female obese subjects was analyzed. A complete nutritional and biochemical evaluation was performed. Serum visfatin levels were measured and to estimate the prevalence of metabolic syndrome, the definitions of the Adult Treatment Panel III was considered RESULTS: Mean age was 48.1 + 12.6 years. Patients were divided in three groups by tertiles of visfatin value, group I (<7.94 ng/ml), group II (7.95-11.78 ng/ml) and group 3 (>11.79 ng/ml). A total of 350 women had metabolic syndrome (42.4%). Values of body mass index, weight, fat mass and waist circumference were lower in patients in the highest tertile group of visfatin than the lowest and middle tertiles of visfatin. Values of C reactive protein were higher in patients in the highest tertile group of visfatin than the lowest and middle tertiles of visfatin. Correlation analysis showed a significant correlation among serum visfatin levels and the independent variables; total cholesterol (r = 0.14;p < 0.05) and C reactive protein (r = 0.12;p < 0.05). In the multivariate analysis, only visfatin concentration increase 0.123 ng/ml (CI95%:0.033-0.445) for each mg/dl of C reactive protein. CONCLUSION: Only C reactive protein remained associated in an independent way. Serum visfatin was not associated with the accumulation of metabolic syndrome factors or the diagnosis of metabolic syndrome in obese female subjects.

Fatty acid-binding protein 2 Ala54Thr genotype is associated with insulin resistance and leptin levels changes after a high monounsaturated fat diet in obese non-diabetic patients.

BACKGROUND: It has been found that the expression of fatty acid binding protein 2 (FABP2) mRNA is under dietary control. This polymorphism was associated with high insulin resistance, and fasting insulin concentrations. OBJECTIVE: The aim of our study was to investigate the influence of Thr54 polymorphism in the FABP2 gene on metabolic response, weight loss and serum adipokine levels secondary to a high monounsaturated fat hypocaloric diet. DESIGN: A sample of 122 obese patients was analyzed in a prospective way. The hypocaloric diet had 1342 kcal, 46.6% of carbohydrates, 34.1% of lipids and 19.2% of proteins, with a 67.5% of monounsaturated fats, and lasted 3 months. RESULTS: Fifty-five patients (45.1%) had the genotype Ala54/Ala54 (wild group) and 67 (64.9%) patients a mutant genotype, Ala54/Thr54 (54 patients, 44.3%) or Thr54/Thr54 (13 patients, 10.7%). In wild group, body mass index (-1.5±1.2 kg/m2), weight (-4.1±3.6 kg), fat mass (-3.6±3.3 kg), waist circumference (-4.9±2.9 cm), insulin (-1.7±3.6 mUI/l), homeostasis model assessment of insulin resistance (HOMA-IR) (-0.6±1.8 units) and leptin levels decreased (-7.6±7.1 ng/ml). In mutant group, anthropometric parameters improved, without changes in biochemical parameters. CONCLUSION: Carriers of Thr54 allele have a different response than wild type obese, with a lack of decrease of insulin levels, leptin levels and HOMA-IR.

Effects of C358A polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) on weight loss, adipocytokines levels, and insulin resistance after a high polyunsaturated fat diet in obese patients.

BACKGROUND AND AIMS: The C385A polymorphism of FAAH gene (rs324420C>A) has been associated with obesity. We investigate the role of this polymorphism on anthropometric and insulin resistance responses to a high polyunsaturated fat hypocaloric diet. METHODS: Obese individuals (no.=99) were assessed at baseline and after 3 months of a high polyunsaturated fat hypocaloric diet. RESULTS: Seventy-one patients (71.7%) had the genotype C385C and 28 (28.3%) patients had the C385A (26 patients, 26.3%) or A358A (2 patients, 2.0%) (A allele carriers group) genotype. In A allele carriers and after dietary intervention, total cholesterol (-16.3 ± 37.4 mg/dl) and LDL-cholesterol (-12.9 ± 6.5 mg/dl) levels decreased. In subjects with C385C genotype, the decreases were significant in total cholesterol (-12.3 ± 27.4 mg/dl), LDL-cholesterol (-7.5 ± 20.5 mg/dl), insulin (-2.2 ± 6.2 mUI/l), and homeostasis model assessment of insulin resistance (HOMA-R) (-0.79 ± 1.15 units) levels. The weight loss was similar in both genotype groups (-4.1 ± 3.8 kg vs -4.2 ± 3.2 kg). Only leptin levels had a significant similar decrease in both genotypes. CONCLUSION: Subjects with C385C genotype of the FAAH showed an improvement on insulin and HOMA-R levels with a high polyunsaturated fat hypocaloric diet after weight loss during 3 months.

Genetic variation in the beta 3-adrenoreceptor gene (Trp64Arg polymorphism) and its influence on anthropometric parameters and insulin resistance under a high monounsaturated versus a high polyunsaturated fat hypocaloric diet.

OBJECTIVE: The aim of our study was to investigate the role of Trp64Arg polymorphism of the beta 3-adrenergic receptor (beta 3-AR) gene on metabolic changes and weight loss secondary to a high monounsaturated fat versus a high polyunsaturated fat hypocaloric diet in obese subjects. MATERIAL AND METHODS: A population of 260 obese subjects was analyzed. In the basal visit, patients were randomly allocated for 3 months to either diet M (high monounsaturated fat hypocaloric diet) or diet P (high polyunsaturated fat hypocaloric diet). RESULTS: There were no significant differences between the positive effects (on weight, body mass index, waist circumference, fat mass) in either genotype group with both diets. With diet P and in genotype Trp64Trp, glucose levels (-6.7 ± 12.1 vs. -1.2 ± 2.2 mg/dl; p < 0.05), total cholesterol (-11.2 ± 8.1 vs. -1.0 ± 7.1 mg/dl; p < 0.05), low-density lipoprotein (LDL) cholesterol (-9.7 ± 10.1 vs. -2.2 ± 8.1 mg/dl; p < 0.05), triglycerides (-11.7 ± 13.1 vs. +1.7 ± 10.3 mg/dl; p < 0.05), homeostasis model assessment for insulin resistance (HOMA-R; -0.7 ± 1.1 vs. -0.3 ± 2.1 units; p < 0.05) and insulin levels (-1.8 ± 4.6 vs. -1.0 ± 9.1 mIU/l; p < 0.05) decreased. CONCLUSION: The metabolic effect of weight reduction by the two hypocaloric diets is greatest in subjects with the normal homozygous beta 3-AR gene. Improvements in total cholesterol, LDL cholesterol, triglyceride, glucose, insulin and HOMA-R levels were better than in the heterozygous group.

Relation of -55CT polymorphism of UCP3 gene with weight loss and metabolic changes after a high monounsaturated fat diet in obese non diabetic patients.

AIMS: The aim of our study was to investigate the influence of -55CT polymorphism of UCP3 gene on metabolic response, weight loss and serum adipokine levels to a high monounsaturated fat hypocaloric diet in obese patients. PATIENTS AND METHODS: A sample of 128 obese patients was analyzed in a prospective way during 3 months. RESULTS: Eighty eight patients (21 males/67 females) (68.8%) had the genotype 55CC (wild genotype group) and 40 patients (8 males/32 females) (31.3%) 55CT (mutant genotype group). In wild genotype group, BMI (-1.6±1.3 kg/m2), weight (-4.3±3.7 kg), fat mass (-3.5±3.3 kg), waist circumference (-5.1±2.9 cm), total cholesterol (-7.2±10.6 mg/dl), LDL cholesterol (-5.3±12.8 mg/dl) and leptin (-4.7±10.1 ng/ml) decreased. In mutant genotype group, BMI (1.3±2.2 kg/m2), weight (-3.0±1.4 kg), fat mass (-2.5±1.1 kg), waist circumference (-2.8±3.1 cm) and leptin (-5.8±10.7 decreased. CONCLUSIONS: In patients with -55CC UCP3 genotype, a high mono-unsaturated hypocaloric diet reduced BMI, weight, waist circumference, waist to hip ratio, fat mass, LDL-cholesterol, total cholesterol and leptin levels. Carriers of T allele had a different response than -55CC patients, with a significant decrease of the same antropometric parameters, but lower than in the wild genotype group, and without significant changes in cholesterol levels.

RS2289487 variation in PERILIPIN gene is a predictor of weight loss and protection against impaired glucose metabolism after a meal-replacement diet in postmenopausal obese females.

OBJECTIVE: The PERILIPIN1 (PLIN1) gene encodes an adipocyte-associated protein that modulates weight. The objective was to evaluate the role of the rs2289487 genetic variant of the PLIN1 gene on weight loss and glucose metabolism secondary to a partial meal replacement (pMR) hypocaloric diet. PATIENTS AND METHODS: We conducted an interventional study in 111 postmenopausal obese females with body mass index (BMI) > 35 kg/m2. The subjects received two intakes per day of a normocaloric hyperproteic formula for 12 weeks. RESULTS: After the pMR diet, body weight, (BMI), fat mass, waist circumference, fasting insulin levels and HOMA-IR decreased in both genotype groups. The improvements in these parameters were higher in C allele carriers than in subjects with TT genotype. The percentage of patients who achieved 7.5% weight loss was higher in the C carriers (57.4% vs. 27.6%), (adjusted Odds Ratio 2.14, 95% CI = 1.33-9.40; p = 0.02). The decrease in the percentage of diabetes mellitus or impaired fasting glucose decrease was statistically significant in C allele carriers (30.2% vs. 18.9%; p = 0.01) (OR 0.54, 95% CI = 0.22-0.78; p = 0.02). CONCLUSIONS: The C allele of rs2289487 predicts the magnitude of weight loss resulting from a pMR diet. These adiposity improvements produce a better improvement in insulin resistance and the percentage of impaired glucose metabolism.

Association of -55CT polymorphism of UCP3 gene with fat distribution, cardiovascular risk factors and adipocytokines in patients with Type 2 diabetes mellitus.

BACKGROUND AND AIMS: Some studies have pointed to a role of uncoupling protein 3 (UCP3) in the regulation of fat distribution. The aim of our study was to investigate the influence of -55CT polymorphism of UCP3 gene on fat mass and adipocytokines in naïve patients with Type 2 diabetes mellitus. DESIGN: A population of 57 patients with Type 2 diabetes mellitus and obesity was analyzed in a cross-sectional study. Genotype of UCP3 gene -55CT was studied. RESULTS: Forty-six patients (80.7%) had the 55CC genotype and 11 patients (19.3%) the 55CT genotype. Fat mass (39.1±15.4 vs 53.3±16.8 kg; p<0.05), weight (92.6±17.7 vs 106.3±17.3 kg; p<0.05), body mass index (36.2±6.5 vs 42.8±5.2 kg/m²; p<0.05), waist circumference (112.8±13.6 vs 127.9±12.3 cm; p<0.05), waist-to-hip ratio (0.96±0.1 vs 1.1±0.2; p<0.05), C reactive protein (6.1±5.1 vs 12.4±6.1 mg/dl; p<0.05) and leptin (92.8±86 vs 114±89 ng/ml; p<0.05) were higher in patients with mutant genotype than in those with wild genotype. CONCLUSION: C reactive protein and fat mass were higher in the mutant group of -55 CT UCP3 gene diabetic patients than in wild type patients.

Interaction of -55CT polymorphism of UCP3 gene with Trp64Arg polymorphism of beta3adrenoreceptor gene on insulin resistance in obese patients.

BACKGROUND: The aim of our study was to investigate the interaction of tryptophan-to-arginine (Trp64Arg) missense mutation in the beta3 adrenoreceptor (Beta3AR) with polymorphism in the UCP3 promotor (-55C->T) on insulin resistance in obese patients. DESIGN: A population of 212 obese patients was analyzed. A bipolar electrical bioimpedance, a biochemical analysis and concentrations of adipocytokines were assessed. RESULTS: One hundred and sixty-two patients (76.4%) had the genotype Trp64/Trp64 (wild type group) and 50 patients Trp64/Arg64 (23.6%) (mutant type group). One hundred and seventy five (87.2%) had the genotype -55CC (wild type group) and 27 patients (22.8%) -55CT (mutant type group). Five patients (2.4%) had both polymorphisms Trp64/Arg64 and -55CT. Patients with one or both mutant genotypes had higher BMI, weight, fat mass, systolic blood pressure and waist circumference than wild type patients. Patients with 55CT or 55CT and Trp64Arg genotype had higher BMI, weight, fat mass, waist circumference, waist to hip ratio glucose, insulin, triglycerides and HOMA than wild type or Trp64Arg mutation. CONCLUSION: Higher concentrations of insulin, HOMA, triglycerides, glucose, BMI, weight, fat mass, waist to hip ratio and waist circumference were observed in patients with -55CT genotype alone or -55CT plus Trp64Arg genotypes than in patients without mutation or only Trp64Arg mutation.

Effect of a commercial hypocaloric diet in weight loss and post surgical morbidities in obese patients with chronic arthropathy, a randomized clinical trial.

INTRODUCTION: The aim of our study was to evaluate in patients with obesity and surgical indication of orthopaedic surgery for chronic osteoarthritis (hip or knee), the impact on weight loss, metabolic control and post surgical co morbidities of a hypocaloric commercial formula (Optisource®) versus conventional nutritional advice before orthopaedic surgery. MATERIALS AND METHODS: 40 patients were randomized in both branches: diet I with lunch and dinner substituted by two Optisource® (1109.3 kcal/day, 166.4 g of carbohydrates (60%), 63 g of proteins (23%), 21.3 g of lipids 17%) and intervention II with nutritional counselling that decreases 500 cal/day of the previous dietary intake. Previous and after 3 months of the treatment, a nutritional and biochemical study was realized. Postsurgical co-morbities have been recorded. RESULTS: 20 patients finished in each group. The improvement in weight (-7.56 ± 5.2 kg vs -5.18 ± 5.1 kg: p < 0.05), body mass index (-3.15 ± 2.2 vs -2.1 ± 1.9 kg/m2: p < 0.05), fat mass (-5.5 ± 5.9 kg vs -3.0 ± 2.6 kg: p < 0.05), insulin (-3.6 ± 3.8 mUI/L vs -3.0 ± 2.6) p < 0.05) and HOMA (-0.5 4 ± 1.2 vs -0.33 ± 1.14): p < 0.05) was higher in group I than in group II. All post surgical recorded parameters such as minutes of orthopaedic surgery, length of stay, vein thrombosis episodes, general infections complications, haemoglobin levels and days till independence of walking were similar in both groups. CONCLUSIONS: Obese patients with chronic osteoarthritis subsidiary of surgery, lose more weight, fat mass and improve more resistance to insulin treated with a mixed diet with a commercial formula hypocaloric that patients treated only with dietary advice.

Lys656Asn polymorphism of leptin receptor, leptin levels and insulin resistance in patients with non alcoholic fatty liver disease.

BACKGROUND: Some studies have pointed to a role of leptin and insulin resistance in pathogenesis of non alcoholic fatty liver disease (NAFLD). The aim of our study was to investigate the influence of Lys656Asn polymorphism LEPR gene on the histological changes, insulin resistance and leptin levels in overweight patients. MATERIAL AND METHODS: A population of 76 patients with NAFLD was recruited in a cross sectional study. A biochemical analysis of serum was measured. Genotype of LEPR gene Lys656Asn was studied. RESULTS: Nineteen patients (25%) had the genotype Lys656Asn and 4 patients genotype Asn656Asn (mutant type group) and 53 patients (69.7%) Lys656Lys (wild type group). Body mass index, weight, fat mass, waist circumference, waist to hip ratio, glucose levels and HOMA-IR were higher in mutant than wild type group. LEPR polymorphism is in any way related with liver lesions. The multivariate analysis adjusted by age, sex, BMI and genotype showed an independently association of lobular inflammation 4.19 (CI95%: 1.37-12.77), portal inflammation 1.97 (CI95%: 1.05-3.74) and steatosis 9.23 (CI95%: 1.47-57.83) with HOMA. Liver steatosis was associated with leptin levels (1.09 (CI95%: 1.06-1.18)), too. CONCLUSION: Lys656Asn polymorphism of LEPR gene is associated with obesity parameters, insulin resistance and glucose levels in patients with NAFLD. In logistic regression analysis, only insulin resistance was associated with portal inflammation), lobular inflammation and steatosis; liver steatosis was related with leptin levels, too.

Relation of G1359A polymorphism of the cannabinoid receptor (CB1) gene with metabolic syndrome by ATP III classification.

BACKGROUND: A polymorphism (1359 G/A) of the cannabinoid type-1 receptor gene was reported as a common polymorphism in Caucasian populations. Some metabolic disorders are related to this polymorphism. OBJECTIVE: The aim of our study was to investigate the association between metabolic syndrome and this polymorphism. DESIGN: A population of 917 obese patients was analysed in a cross-sectional survey. Bioimpedance, blood pressure, an assessment of nutritional intake and biochemical analysis were recorded. RESULTS: Five hundred and twelve patients (55.8%) had the genotype G1359G (wild-type group), whereas 344 (37.5%) had genotype G1359A and 61 (6.7%) patients had A1359A. (G1359A and A1359A were included in the mutant-type group; 44.2% total). In wild type patients, metabolic syndrome prevalence was higher (54.9% versus 45.1%; p < 0.05) than no metabolic syndrome prevalence. In patients with mutant genotypes, metabolic syndrome prevalence was lower (43.7% versus 56.3%; p < 0.05). Glucose, insulin and homeostasis model assessment levels were higher in patients with the wild genotype than in those with the mutant type. Adiponectin levels were lower in patients with the wild genotype than in those with the mutant type. CONCLUSION: The novel finding of this study is the association of the G1359A and A1359A cannabinoid type-1 genotypes with a lower prevalence of metabolic syndrome than the G1359G genotype.

Resistin levels in morbid obese patients following the biliopancreatic diversion surgery.

Previous studies addressing the changes of resistin concentrations in morbidly obese patients after bariatric surgery have yielded conflicting results. The purpose of the present study was to investigate the changes in serum resistin levels 1 year after biliopancreatic diversion in morbidly obese patients without diabetes mellitus. A cohort of 39 morbidly obese patients without diabetes mellitus was operated. Biochemical and anthropometric evaluation were realized at basal visit and at each visit. The frequency of patients with hypertension and hyperlipidemia was recorded at each visit. Overall the mean patient age was 44.8 ± 14.1, and the mean preoperative BMI was 47.3 ± 6.5 kg/m². After one year of surgery, a significant decrease was observed in BMI, weight, waist circumference, fat mass, blood pressure, total cholesterol, LDL cholesterol, and triglyceride levels. Resistin levels did not change after surgery (5.61 ± 1.93 ng/ml vs. 6.41 ± 3.58 ng/ml; ns). Correlation analysis showed a positive association between basal resistin and weight (r = 0.68, p < 0.01) and fat mass (r = 0.65, p < 0.05). Resistin concentrations did not change after massive weight loss with biliopancreatic diversion in morbid obese patients without diabetes mellitus.

The serum profile of adipokines in naïve patients with diabetes mellitus type 2 and obesity.

BACKGROUND: The aim of this study was to explore the relationship of serum profile of adipokines with cardiovascular risk factors and anthropometric parameters in patients with diabetes mellitus type 2. SUBJECTS: A population of 108 obese patients with DM2 was analyzed. A complete biochemical anthropometric and nutritional evaluation was performed. RESULTS: In the analysis with leptin as a dependent variable, the IL-6 and glucose levels remained in the model (F = 6.2; P<0.05), with an increase of 5.8 (CI 95%:2.7-7.6) ng/ml with each 1 pg/ml of IL-6 and of 5.2 (CI95%:2.5-5.8) ng/ml with each 1 mg/dl of glucose. In a second model with adiponectin as a dependent variable, the BMI remained in the model (F = 3.77;P<0.05), with an decrease of -3.77 (CI 95%:0.53-7.1) ng/ml with each 1 point of BMI. In the third multivariate analysis with IL-6 as a dependent variable, the glucose level remained in the model (F = 10.1; P<0.01), with an increase of 0.09 (CI95%:0.06-0.12) pg/ml with each 1 mg/dl of glucose. In the fourth multivariate analysis with resistin as a dependent variable, the CRP remained in the model (F = 2.51; P<0.05), with an increase of 0.28 (CI 95%:0.08-0.48) pg/ml with each 1 mg/dl of CRP. CONCLUSION: Serum profile of adipokines is associated with different risk factors in diabetic obese patients.

Lys656Asn polymorphism of leptin receptor gene and metabolic syndrome in obese patients.

BACKGROUND: The etiology of common obesity is complex, because many genetic, environmental and metabolic factors might act. Alterations of the normal leptin receptor gene be involved in the development of obesity. The polymorphism on codon 656 produces a change in charge, making this change a possibility to be functional. OBJECTIVE: The aim of our study was to investigate the relationship between metabolic syndrome and Lys656Asn polymorphism in obese patients. DESIGN: A population of 714 obese patients (body mass index > 30) was analyzed in cross-sectional survey. A bioimpedance, blood pressure, a serial assessment of nutritional intake with 3 days written food records and biochemical analysis were performed. RESULTS: Four hundred and seventy eight patients (66.9%) had the genotype Lys656/Lys 656 (wild group), whereas 236 (33.1%) had either the genotype Lys656/Asn656 (212 patients, 29.7%) or the genotype Asn656/Asn656 (24 patients, 3.4%) (mutant group). Prevalence of metabolic syndrome (MS) with ATP III definition was 49.4% (353 patients; 35.1% males and 64.9% females) and 50.6% patients without MS (n = 361; 25.2% males and 75.8% females). Prevalence of leptin receptor (LEPR) genotypes was similar in patients with metabolic syndrome (65.5% wild genotype and 34.5% mutant genotype) and without metabolic syndrome (68.3% wild genotype and 31.7% mutant genotype). No differences in anthropometric and biochemical parameters were detected between genotypes in the same group of metabolic syndrome. CONCLUSION: The finding of our study is the lack of association of the Lys656/Asn656 and Asn656/ Asn656 genotypes with metabolic syndrome.

Effect of a probiotic on liver aminotransferases in nonalcoholic fatty liver disease patients: a double blind randomized clinical trial.

OBJECTIVE: The present pilot trial was carried out to evaluate the effects of an acute treatment with a mixture containing 500 million of Lactobacillus bulgaricus and Streptococcus thermophilus per day in patients with non alcoholic fatty liver disease (NAFLD). RESEARCH METHODS: A sample of 30 patients with NAFLD (diagnosed by liver biopsy) was enrolled and 28 patients were analyzed in a double blind randomized clinical trial. Patients were randomized to one of the following treatments during 3 months: group I, treated with one tablet per day with 500 million of Lactobacillus bulgaricus and Streptococcus thermophilus and group II, treated with one placebo tablet (120 mg of starch). RESULTS: In group I, alanine amino transferase (ALT: 67.7 +/- 25.1 vs. 60.4 +/- 30.4 UI/L; p < 0.05), aspartate aminotransferase activity (AST: 41.3 +/- 15.5 vs. 35.6 +/- 10.4 UI/L; p < 0.05) and gammaglutamine transferase levels (gammaGT: 118.2 +/- 63.1 vs. 107.7 +/- 60.8 UI/L; p < 0.05) decreased. In group II, all liver function parameters remained unchanged (ALT: 60.7 +/- 32.1 vs. 64.8 +/- 35.5 UI/L; p < 0.05), aspartate aminotransferase activity (AST: 31.7 +/- 13.1 vs. 36.4 +/- 13.8 UI/L; ns) and gammaglutamine transferase levels (gammaGT: 82.1 +/- 55.1 vs. 83.6 +/- 65.3 UI/L; ns). Anthropometric parameters and cardiovascular risk factors remained unchanged after treatment in both groups. CONCLUSION: A tablet of 500 million of Lactobacillus bulgaricus and Streptococcus thermophilus, with a randomized clinical design, improved liver aminotransferases levels in patients with NAFLD.