Dietary acid load and its interaction with CETP TaqB1 polymorphisms on lipid profile among patients with Type 2 diabetes mellitus.

OBJECTIVE: Gene-diet interaction plays a key role in the inter-individual differences in lipid abnormalities as a major risk factor for cardiovascular diseases (CVDs). Thus, we explored the interaction between CETP TaqB1 polymorphism with dietary acid load (DAL) on lipid profile among type 2 diabetes mellitus (T2DM). METHOD: This cross-sectional study conducted on 220 Iranian patients with T2DM. Dietary acid load (PRAL and NEAP) was calculated via a validated food-frequency questionnaire (FFQ). The polymerase chain reaction (PCR) used for genotyping Taq1B polymorphism. Biochemical markers were measured by standard protocol. The interaction between CETP Taq1B polymorphism and DAL (PRAL and NEAP) on lipid profile was performed by a generalized linear regression model (GLM). RESULTS: The overall prevalence of rs708272 genotypes was 8.6%, 72.7% and 18.6% for B1B1, B1B2 and B2B2 genotype respectively. This study showed that people with the B1B1 genotype had greater LDL, TC, LDL/HDL, and TG when they consumed diets that scored higher on the NEAP and PRAL indexes than those with the B1B2 and B2B2 genotypes. Besides, carriers of the B1B1 allele who were in the highest tertile of NEAP, had lower HDL (P Interaction < 0.05). CONCLUSIONS: In summary, the lipid profile might be improved in B1B1 homozygotes by less adherence to DAL indexes, however, the findings should be validated in high-quality interventional studies.

Interactions of BDNF Val66met and dietary indices in relation to metabolic markers among patient with type 2 diabetes mellitus: a cross-sectional study.

BACKGROUND: Gene-diet interaction is related to the progression of diabetes and cardiovascular diseases biomarkers. We aimed to evaluate the interaction between diet quality indices and BDNF Val66Mat (rs6265) on cardiometabolic markers among diabetic patients. METHODS: This cross-sectional study was conducted on 634 patients with type 2 diabetes mellitus, which were randomly recruited from diabetic centers in Tehran. Dietary intakes were estimated by a previously validated semi-quantitative food frequency questionnaire comprising 147 items. All participants were categorized into three categories, based on healthy eating index (HEI), diet quality index (DQI), and phytochemical index (PI) scores. Polymerase chain reaction was used for genotyping the BDNF Val66Met. Interactions were tested using analysis of covariance in adjusted and crude models. RESULTS: Our result showed that higher DQI, HEI, and PI scores significantly decrease body mass index and waist circumference among individuals with Met/Met, Val/Met, and Val/Val genotypes (P interactions < 0.05). Moreover, the highest quartile of the DQI and PI, compared to the lowest, showed lower TG level among Met allele carriers compared to Val/Val homozygotes (P interaction = 0.004 and 0.01, respectively) and a faster reduction in IL-18 and TC level was seen among Met/Met, Val/Met who had higher HEI intake than those with Val/Val genotype. CONCLUSIONS: BDNF Val66Met polymorphism may interact with HEI, DQI, and PI. We have revealed that Met allele acts as a protective allele for diabetic patients and may have a beneficial influence on cardio-metabolic factors through regulating dietary intake.

Dietary acid load modifies the effects of ApoA2-265 T > C polymorphism on lipid profile and serum leptin and ghrelin levels among type 2 diabetic patients.

This investigation with aimed the effect of APOA2-265 T > C polymorphism and dietary acid load (DAL) as either potential renal acid load (PRAL) and net endogenous acid production (NEAP) intake interaction on metabolic markers in type 2 diabetes mellitus (T2DM). In present cross-sectional study, 737 patients with T2DM (290 men and 447 women) were enlisted from diabetes centers in Tehran. The dietary intakes of all participants during the last year was acquired by a validated semi-quantitative food frequency (FFQ) questionnaire. Polymerase chain reaction (PCR) was used for genotyping the APOA2-265 T > C. Biochemical indises containing leptin, ghrelin, total cholesterol (Bailey et al., J Clin Invest 97:1147-1453, 1996), low-density lipoprotein cholestrol (LDL-C), high-density lipoprotein cholestrol (HDL-C), triglyceride (TG), superoxide dismutase (SOD), high sensitivy C-reactive protein (hs-CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), prostaglandin F2α (PGF2α) and interleukin 18 (IL18) were measured by standard method. Atherogenic indices (AIP, AC, CR-I, CR-II) were calculated. The gene-diet interactions were evaluated using an GLM. The frequency overall prevalence of rs5082 genotypes was 63.82 and 36.17% for T-allele and C-allele respectively. TG, Ghrelin, and hs-CRP concentrations were significantly higher among carriers with C allele than TT homozygotes. However, TC/CC genotypes have lower PTX3 than TT homozygotes (P < 0.05). C-allele carriers had highest mean of BMI (PNEAP=0.04, PPRAL = 0.006), WC (PNEAP=0.04, PPRAL = 0.04), TC (PNEAP=0.03, PPRAL = 0.01), ghrelin (PNEAP=0.01, PPRAL = 0.04), and leptin (PNEAP=0.04, PPRAL = 0.03) when placed in top tertiles of NEAP and PRAL.BMI, WC, TC, ghrelin, and leptin levels may be modified in C carriers by decreasing DAL, though, further investigations are required to confirm these findings.

Macronutrient intake modulates impact of EcoRI polymorphism of ApoB gene on lipid profile and inflammatory markers in patients with type 2 diabetes.

We sought to examine whether dietary intakes may affect the relationship between ApoB EcoRI and lipid profile, as well as serum inflammatory markers, in patients with type 2 diabetes (T2DM). This current study consisted of 648 diabetic patients. Dietary intake was calculated by a food frequency questionnaire. Biochemical markers (high-density lipoprotein (HDL), total cholesterol (TC), LDL, TG, CRP, IL-18, PGF2α) were measured based on standard protocols. Genotyping of the Apo-B polymorphisms (rs1042031) was conducted by the PCR-RFLP method. The gene-diet interactions were evaluated using GLMs. In comparison to GG homozygotes, A-allele carriers with above the median -CHO intake (≥ 54 percent of total energy) had considerably greater TC and PGF2a concentrations. Furthermore, as compared to GG homozygotes, A-allele carriers with above the median protein intake (≥ 14 percent of total energy) had higher serum levels of TG (P = 0.001), CRP (P = 0.02), TG/HDL (P = 0.005), and LDL/HDL (P = 0.04) ratios. Moreover, A-allele carriers with above the median total fat intake (≥ 35 percent of total calories) had significantly higher TC level (P = 0.04) and LDL/HDL (P = 0.04) ratios compared to GG homozygotes. Furthermore, when compared to GG homozygotes, A-allele carriers who consumed above the median cholesterol (> 196 mg) had greater TG (P = 0.04), TG/HDL (P = 0.01) ratio, and IL-18 (P = 0.02). Furthermore, diabetic patients with the GA, AA genotype who consume above the median cholesterol had lower ghrelin levels (P = 0.01). In terms of LDL/HDL ratio, ApoB EcoRI and dietary intakes of specific fatty acids (≥ 9 percent for SFA and ≥ 12 percent for MUFA) had significant interaction. LDL/HDL ratio is greater in A-allele carriers with above the median SFA intake (P = 0.04), also when they consumed above the median MUFA this association was inverse (P = 0.04). Our study showed that plasma lipid levels in participants carrying the (AA or AG) genotype were found to be more responsive to increasing the percentage of energy derived from dietary fat, CHO, protein, SFA, and cholesterol consumption. Therefore, patients with a higher genetic susceptibility (AA or AG) seemed to have greater metabolic markers with a higher percentage of macronutrient consumption. Also, ApoB EcoRI correlations with metabolic markers might be attenuated with above the median MUFA consumption.

A personalised diet approach study: Interaction between PPAR-γ Pro12Ala and dietary insulin indices on metabolic markers in diabetic patients.

BACKGROUND: The present study aimed to investigate the effect of the interaction between peroxisome proliferator-activated receptor gamma (PPAR-γ) Pro12Ala polymorphisms and dietary insulin load and insulin index (DIL and DII) on cardio-metabolic markers among diabetic patients. METHODS: This cross-sectional study was conducted on 393 diabetic patients. A food-frequency questionnaire was used for DIL and DII calculation. PPAR-γ Pro12Ala was genotyped by a polymerase chain reaction-restriction fragment length polymorphism method. Biochemical markers, including total cholesterol, low-density lipoprotein, high-density lipoprotein, triglyceride, superoxide dismutase, C-reactive protein, total antioxidant capacity, pentraxin-3, isoprostaneF2α, interleukin-18, leptin and ghrelin, were measured by a standard protocol. RESULTS: Risk-allele carriers (CG, GG) had higher obesity indices [body mass index (pinteraction = 0.006) and WC (pinteraction = 0.04)] compared to individuals with the CC genotype when they consumed a diet with higher DIL and DII respectively. Besides, carriers of the G-allele who were in the highest tertile of DIL had lower high-density lipoprotein (pinteraction = 0.04) and higher isoprostaneF2α (pinteraction = 0.03) and pentraxin-3 (pinteraction = 0.03). Moreover, the highest tertile of the DII, showed an increase in interleukin-18 (pinteraction = 0.01) and lower superoxide dismutase (pinteraction = 0.03) for risk-allele carriers compared to those with CC homozygotes. CONCLUSIONS: We revealed that the PPAR-γ Pro12Ala polymorphism was able to intensify the effect of DIL and DII on cardiovascular disease risk factors; risk-allele carriers who consumed a diet with high DIL and DII score were more likely to be obese and have higher inflammatory markers. Also, protective factors against cardiovascular disease risk factors were reduced significantly in this group compared to CC homozygotes.

Deletion allele of Apo B gene is associated with higher inflammation, oxidative stress and dyslipidemia in obese type 2 diabetic patients: an analytical cross-sectional study.

BACKGROUND: We decided to compare some inflammatory, and oxidative stress markers, as well as lipid profiles between the obese and non-obese patients with type 2 diabetes considering ApoB gene polymorphism. METHODS: one-hundred sixty two patients with type 2 diabetes were included in this study. ApoB genotyping was conducted by the polymerase chain reaction. Serum interleukin-(IL-18), pentraxin-3 (PTX-3), and high sensitive- C reactive protein (hs-CRP) was measured as the inflammatory markers. Moreover, copper-zinc superoxide dismutase (Cu/Zn-SOD), total antioxidant capacity (TAC) and 8-isoprostane F2α were analyzed for oxidative stress assessment. Anthropometric indices and lipid profiles were measured. RESULTS: Adjusted for confounders, serum hs-CRP (p = 0.04), LDL-C (p = 0.01), LDL-C/HDL-C (p = 0.04), and TG (p = 0.02) were significantly lower at the Homozygous Insertion (Ins)/Ins vs. deletion (Del) allele carriers in the obese patients. Serum TAC was significantly lower at the obese Del allele carriers than Ins/Ins Homozygous (p = 0.03). Serum hs-CRP (p = 0.006), and 8-IsoprostanF2α (P = 0.04) were significantly higher in the obese Del allele carriers than non-obese. Serum Cu/Zn-SOD was significantly higher in the non-obese Del allele carriers than obese (p = 0.04). CONCLUSION: Inflammation, dyslipidemia, and oxidative stress are higher in the Obese Del allele carriers with type 2 diabetes which prone them to other chronic disorders.

Interaction between Apo A-II -265T > C polymorphism and dietary total antioxidant capacity on some oxidative stress and inflammatory markers in patients with type 2 diabetes mellitus.

This work aims to examine the interaction between apo A2 (Apo A-II) -265T > C SNP and dietary total antioxidant capacity (DTAC) on inflammation and oxidative stress in patients with type 2 diabetes mellitus. The present cross-sectional study included 180 patients (35-65 years) with identified Apo A-II genotype. Dietary intakes were assessed by a FFQ. DTAC was computed using the international databases. IL-18 (IL18), high-sensitivity C-reactive protein (hs-CRP), pentraxin (PTX3), serum total antioxidant capacity (TAC), superoxide dismutase (SOD) activity and 8-isoprostaneF2α (PGF2α) markers were obtained according to standard protocols. General linear model was used to evaluate the interaction. The interaction of gene and DTAC (PFRAP = 0·039 and PORAC = 0·042) on PGF2α level was significant after adjusting for confounders. A significant interaction was observed on IL18 level (PORAC = 0·018 and PFRAP = 0·048) and SOD (PTEAC = 0·037) in obese patients. Among patients whose DTAC was higher than the median intake, the levels of hs-CRP and PGF2α were significantly higher only in individuals with CC genotype. Serum TAC (PFRAP = 0·030, PORAC = 0·049) and SOD were significantly lower in the CC genotype. There was a favourable relationship between the high-DTAC and SOD (obese: PTEAC = 0·034, non-obese: PFRAP = 0·001, PTRAP < 0·0001, PTEAC = 0·003 and PORAC = 0·001) and PGF2α (non-obese: PORAC = 0·024) in T-allele carriers. The rs5082 SNP interacts with DTAC to influence several cardiometabolic risk factors. Also, we found dietary recommendations for antioxidant-rich foods intake might be useful in the prevention of diabetes complications in the T carrier more effectively than the CC genotype. Future large studies are required to confirm these results.

Interactions of dietary insulin index and dietary insulin load with brain-derived neurotrophic factor (BDNF) Val66Met polymorphism in relation to cardiometabolic markers in Iranian diabetic patients: a cross-sectional study.

The progression of cardiometabolic diseases is determined by both genetic and environmental factors. Gene-diet interactions may therefore be important in modulating the risks of developing metabolic diseases. The objectives were to investigate the effect of the interaction between brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms and dietary insulin index (DII) and dietary insulin load (DIL) on cardiometabolic markers among diabetic patients. In this cross-sectional study, blood samples were collected from 667 patients. DIL and DII were defined using a validated FFQ. Genotyping the BDNF Val66Met polymorphism was conducted by the PCR-Restriction fragment length polymorphism (RFLP) method. Interactions between dietary indices and gene variants were evaluated using a generalised linear model. PGF2a concentrations were significantly higher among Val homozygotes than Met-allele carrier. This study revealed that, compared with individuals with the Val/Val genotype, those with the Met/Val or Met/Met genotype had lower BMI (Pinteraction = 0·04), TAG (Pinteraction = 0·04), leptin (Pinteraction = 0·01), LDL (Pinteraction = 0·04) and total cholesterol (Pinteraction = 0·01) when they consumed diets higher on the DIL index. Moreover, the highest quartile of the DIL, compared with the lowest, showed increase in waist circumference (Pinteraction = 0·02) and LDL/HDL (Pinteraction = 0·04) for Val/Val homozygotes compared with Met-allele carriers. BDNF Val66Met variants may interact with DIL and DII, thus be involved in the development of cardiometabolic risk factors. If diabetic patients with Met alleles regulate dietary intakes, they have a protective opportunity to regulate their cardiometabolic markers.

ApoA2-256T > C polymorphism interacts with Healthy Eating Index, Dietary Quality Index-International and Dietary Phytochemical Index to affect biochemical markers among type 2 diabetic patients.

Several investigations revealed the association between ApoA2 concentration and lipid profile, inflammation and oxidative stress markers. Dietary habits also play a major role in the health status of individuals with type 2 diabetes mellitus (T2DM). This study aimed to investigate the interaction of ApoA2-256T > C with dietary indexes on ghrelin and leptin hormones together with biochemical markers among individuals with T2DM. A cross-sectional study was conducted on 726 randomly selected individuals with T2DM. A validated FFQ was used to evaluate Healthy Eating Index, Dietary Quality Index-International (DQI-I) and Dietary Phytochemical Index (DPI). ApoA2-256T > C genotypes were detected by real-time-PCR. Ghrelin, leptin and biochemical markers were also assessed. ANCOVA was used for the interaction between the polymorphism and dietary indexes. A significant interaction was observed between ApoA2-256T > C and DQI-I on high-sensitivity C-reactive protein (hs-CRP) level and superoxide dismutase (SOD) activity. Besides, the interaction of the SNP and DPI significantly affected hs-CRP and 8-isoprostane F2α (PGF2α) levels. CC in the second tertile of DPI had the lowest hs-CRP level, and it was elevated due to adhering to DQI-I (Pinteraction = 0·01 and 0·04, respectively). Moreover, T-allele (protective allele) carriers with the highest level of PGF2α and SOD activity were those in the second tertile of DPI and DQI-I, respectively (Pinteraction = 0·03 and 0·007, respectively). SOD activity, hs-CRP and PGF2α concentration may be modified in T-allele carriers and CC by the adherence to DPI and DQI-I, though additional studies are required to confirm these findings.

Interaction between CETP Taq1B polymorphism and HEI, DQI and DPI on metabolic biomarkers in patients with type 2 diabetes.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a multidimensional consequence of environmental and genetic factors. Cholesteryl ester transfer protein (CETP) Taq1B polymorphism has been reported as a main predictor of dyslipidaemia, comprising an important complication in persons with T2DM. However, diet could affect T2DM patients metabolic health. METHODS: We investigated the combination of gene-diet effects on some metabolic biomarkers. In our cross-sectional study, blood samples of 220 patients were collected. Dietary indices (healthy eating index, dietary quality index and dietary phytochemical index) were obtained from a validated semi-quantitative food frequency questionnaire. CETP Taq1B polymorphism was genotyped by a polymerase chain reaction-restriction fragment polymorphism method. Data were analysed by analysis of covariance. RESULTS: The interaction between the CETP Taq1B polymorphism and dietary indices on low density lipoprotein/high density lipoprotein was significant (p < 0.001 both crude and adjusted models). In addition, the interaction between polymorphism and dietary quality index on total antioxidant capacity (p = 0.004 crude model, p = 0.005 after adjusting) and pentraxin 3 (p = 0.01 both crude and adjusted models) was significant. Also, the interaction between polymorphism and healthy eating index on waist circumference (p = 0.005 both crude and adjusted models) and dietary phytochemical index on interleukin-18 (p = 0.03 crude model) was significant. CONCLUSIONS: Our results indicated the effect of CETP Taq1B polymorphism on some inflammatory and anthropometrics markers (total antioxidant capacity, pentraxin 3, interleukin-18, low density lipoprotein/high density lipoprotein and waist circumference) with high and low adherence to dietary incides.

Dietary quality indices modify the effects of apolipoprotein B polymorphisms on biochemical and anthropometric factors in type 2 diabetes mellitus.

We tried to identify the interaction between dietary quality indices and apolipoprotein B Ins/Del and EcoR1 polymorphisms on biochemical and anthropometric factors in patients with type 2 diabetes mellitus (T2DM). This cross-sectional study recruited 700 adults with T2DM in Tehran. The genotypes of Ins/Del and EcoR1 single nucleotide polymorphisms (SNP) were explored via polymerase chain reaction (PCR). Dietary quality index-international (DQI-I), healthy eating index-2015 (HEI-2015) and dietary phytochemical index (DPI) were calculated by semi-quantitative food frequency questionnaire (FFQ). In both crude and adjusted model for confounding factors, we observed significant interactions between DQI-I and Ins/Del SNP on leptin in and 8-iso-prostaglandin F2 α (8-iso-PGF2α), DPI and EcoR1 SNP on total cholesterol (TC) and between Ins/Del SNP and HEI-2015 on interleukin-18 (IL-18). Furthermore, in crude model there were close to meaningful interactions between EcoR1 SNP and DQI-I on total antioxidant capacity (TAC) and between EcoR1 SNP and HEI-2015 on serum leptin and superoxide dismutase (SOD) levels. Our finding indicated that the association between DQI-I, HEI-2015 and DPI with IL-18, TC, leptin and 8-iso-PGF2α in patients with T2DM might be dependent on Ins/Del and EcoR1 variants in ApoB gene.

The interactions between dietary fats intake and Caveolin 1 rs 3807992 polymorphism with fat distribution in overweight and obese women: a cross-sectional study.

BACKGROUND: It has been reported that dietary fats and genetic factors in individuals are associated with the pattern of fat distribution. This study aimed to evaluate the interaction between dietary fats intake and Caveolin1 (CAV-1) rs 3807s992 polymorphism with fat distribution in overweight and obese women. METHODS: A total of 221 participants were included in the current cross-sectional study. Body composition, biochemical parameters were evaluated by body composition analyzer and Pars Azmoon kits and genotypes determination was performed by PCR-RFLP, dietary fats were measured using a validated semi-quantitative food frequency questionnaire (FAQ). RESULTS: The frequency of GG, AA and AG genotypes were 53.1, 24.6, and 22.3%, respectively, and the mean intake of total dietary fat intake was 97.47 ± 36.87 g. There was positive significant interaction between total fat intake and AA genotype on visceral fat level (p = 0.001), trunk fat (p = 0.01) and waist circumference (p = 0.05), positive significant interaction between total fat intake and AG genotype on the waist to hip ratio (WHR) (p = 0.02) and visceral fat level (p = 0.05), positive borderline significant interaction between saturated fatty acid and AA genotype on the trunk fat (p = 0.06), and between trans-fatty acids and AG genotype on WHR (p = 0.04), visceral fat level (p = 0.01), and between monounsaturated fatty acid and AG genotype on WHR (p = 0.04), and a borderline interaction between polyunsaturated fatty acid and AA genotypes on visceral fat level (p = 0.06), negative significant interaction between AG genotypes and linolenic acid on WHR (p = 0.04), borderline significant interaction between ALA and AG genotype on WHR (p = 0.06). CONCLUSIONS: Our findings showed that CAV-1 rs 3807992 polymorphism and dietary fats were associated with fat distributions in individuals.

Interaction between dietary total antioxidant capacity and BDNF Val66Met polymorphism on lipid profiles and atherogenic indices among diabetic patients.

Brain-derived neurotrophic factor (BDNF) belongs to the "neurotrophin" family of growth factors, and it has recently been associated to cardiovascular disease (CVD). We anticipated that BDNF Val66Met polymorphisms may alter CVD risk markers such as serum lipid profile differences, and interaction with total antioxidant capacity of diet (DTAC) could alter these clinical parameters. This cross-sectional study consisted of 667 diabetic patients (39.7% male and 60.3% female). DTAC was calculated by international databases. Biochemical markers including total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), superoxide dismutase (SOD), C-reactive protein (CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), isoprostaneF2α (PGF2α). interleukin 18 (IL18), leptin and ghrelin were measured by standard protocol. Atherogenic indices (AIP, AC, CR-I, CR-II) were calculated. Genotyping of the BDNF Val66Met polymorphisms was conducted by the real-time PCR-RFLP method. The gene-diet interactions were evaluated using a generalized linear mode (GLMs). Carriers of the Val/Met genotype who were in the higher median intake of FRAP had lower HDL (P:0.04) and higher TG (P:0.005), AIP (P:0.02) and AC (P:0.02) index compared to Val/Val genotypes with lower median intake. Moreover, diabetic patients with Val/Met genotype who consumed higher ORAC intake had increased odds for anthropometric indices (BMI (P:0.01) and WC (P:0.03)), lipid profiles (TG) (P:0.01), and atherogenic index (AIP) (P:0.02), also decreased odds for HDL (P:0.03) concentration compared to reference group whit lower ORAC intake. Individuals with Val/Met genotype who consumed higher TRAP intake had increased odds for WC (P:0.04), TC (P:0.001), TG (P < 0.001), AIP (P < 0.001) and AC (P < 0.001). Finally, Val/Met patients with a higher median intake of TEAC had higher TG (P:0.02), AIP (P:0.009) and AC (P:0.03) compared to the reference group whit lower TEAC intake. Our study showed that Val/Met genotype had also the highest lipid profile and atherogenic indices even in the highest adherence to DTAC. While it seems that the presence of the Val/Val wild-type and BDNF Met/Met homozygotes in diabetic patients with a high DTAC is a protective factor.

Interactions between caveolin 1 polymorphism and the Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay diet (MIND) diet on metabolic dyslipidemia in overweight and obese adult women: a cross-sectional study.

OBJECTIVE: The increased prevalence of metabolic dyslipidemia (MD) and its association with a variety of disorders raised a lot of attention to its management. Caveolin 1 (CAV1) the key protein in the caval structure of plasma membranes is many cell types that play an important role in its function. (CAV1) is a known gene associated with obesity. Today, a novel diet recognized as the Mediterranean and Mediterranean-DASH Intervention for Neurodegenerative Delay diet (MIND) is reported to have a positive effect on overall health. Hence, we aimed to investigate the interactions between CAV1 polymorphism and MIND diet on the MD in overweight and obese patients. RESULTS: Remarkably, there was a significant interaction between the MIND diet and CAV1 rs3807992 for dyslipidemia (ß = - 0.25 ± 132, P = 0.05) in the crude model. Whereby, subjects with dominant alleles had a lower risk of dyslipidemia and risk allele carriers with higher adherence to the MIND diet may exhibit the lower dyslipidemia. This study presented the CAV1 gene as a possible genetic marker in recognizing people at higher risks for metabolic diseases. It also indicated that using the MIND diet may help in improving dyslipidemia through providing a probable interaction with CAV1 rs3807992 polymorphism.

The effect of dietary total antioxidant capacity (DTAC) and Caveolin-1 gene variant interaction on cardiovascular risk factors among overweight and obese women: A cross-sectional investigation.

BACKGROUND: Previous studies have shown that the Caveolin-1 (CAV-1) gene variant may be associated with Cardiovascular disease (CVD) risk. Moreover, dietary total antioxidant capacity (DTAC) has been shown to potentially elicit favorable effects on CVD risk. Therefore, this study sought to investigate the effect of DTAC and CAV-1 interaction on CVD risk factors. METHODS: This cross-sectional study consisted of 352 women, with overweight and/or obesity, aged 18-48years from Iran. A food frequency questionnaire (FFQ), with 147 items, was used to assess dietary intake. The CAV-1 rs 3807992 and anthropometric data were measured by the PCR-RFLP method and bioelectrical impedance analysis (BIA), respectively. Serum profiles were measured by standard protocols. Participants were also divided into two groups based on DTAC score and rs3807992 genotype. RESULTS: The mean age of the participants was 37.34 ± 9.11 and 36.01 ± 9.12 years for homozygous (GG) and minor allele carriers (AG + AA) respectively.The mean ± SD of insulin, total cholesterol (TC),high-density lipoprotein (HDL), low-density lipoprotein (LDL) and TG of participants were 1.21 ± 0.23, 185.3 ± 35.77, 46.58 ± 10.86, 95.3 ± 24.12 and 118.1 ± 58.88, respectively. There was a significant difference between genotypes for physical activity (P = 0.05), HDL (P < 0.001), insulin (P = 0.04), CRI-I (TC/HDL-C) (P = 0.01), and CRI-II (LDL-C/HDL-C) (P = 0.04). Our findings also showed, after controlling for confounding factors, significant interactions between DTAC score and the A allele carrier group on TC (Pinteraction = 0.001), LDL (Pinteraction = 0.001), insulin (Pinteraction = 0.08), HOMA-IR (Pinteraction = 0.03), AC ((TC - HDL - C)/HDL - C) (Pinteraction = 0.001), and CHOLINDEX (LDL-C-HDL-C) (Pinteraction = 0.02). CONCLUSION: The results of the present study indicate that high DTAC intake may modify the odds of risk factors for CVD in AA and AG genotypes of rs 3807992. These results highlight that diet, gene variants, and their interaction, should be considered in CVD risk assessment.

Interaction between CETP polymorphism and dietary insulin index and load in relation to cardiovascular risk factors in diabetic adults.

Gene-diet interactions may play an important role in the inter individual diversity observed in on cardiovascular disease (CVD) risk factors. Therefore, in the current study, we examined the interaction of CETP TaqB1 polymorphism with dietary insulin index and load (DII and DIL), in altering on CVD risk factors among type 2 diabetes mellitus (T2DM). In this cross-sectional study, blood samples were collected from 220 type 2 diabetic patients (134 females and 86 male) with a mean age of 52.24 years in Tehran, Iran. DIL and DII were obtained via validated food-frequency questionnaire (FFQ). Taq1B polymorphism was genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Biochemical markers including total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), superoxide dismutase (SOD), C-reactive protein (CRP), total antioxidant capacity (TAC), pentraxin-3 (PTX3), isoprostaneF2α (PGF2α). interleukin 18 (IL18), leptin and ghrelin were measured by standard protocol. Patients with B1B1 genotype had lower lipid profiles include LDL/HDL (P < 0.001) and TG (P = 0.04) when they consumed diets higher on the DIL and DII index. Moreover, carriers of B2B2 genotype who were in the last tertile of DIL had higher antioxidant and inflammatory markers include SOD (P = 0.01), PGF2α (P = 0.04) and CRP (P = 0.02). Further, a significant interaction between CETP TaqB1 and DII was shown in terms of WC (P = 0.01), where the highest WC were observed in B2B2 genotype carriers following a DII score. However, the highest inflammatory and antioxidant markers include CRP (P = 0.04), TAC (P = 0.01), SOD (P = 0.02), and PGF2α (P = 0.02) were observed in B2B2 genotype carriers when they consumed diets higher on the DII index. Based on the current study, it could be proposed that CETP polymorphism may be associated with CVD risk factors in T2DM patients with high following insulin indices, including DII and DIL. It seems that CETP Taq1B polymorphism can invert the result produced by insulin. This conclusion illustrates that the CETP Taq1B B1 allele could counteract the CVD risk induced by high DII and DIL.

Interactions between Caveolin-1 (rs3807992) polymorphism and major dietary patterns on cardio-metabolic risk factors among obese and overweight women.

BACKGROUND: Caveolin-1 (CAV-1) is a cholesterol-dependent essential component located in caveolae. Several studies have been CAV-1 related to cardio-metabolic parameters in animal models, however, there are few studies in humans. Importantly, there is no study has investigated the interaction between CAV-1 rs3807992 gene and dietary patterns (DPs) on cardio-metabolic risk factors. METHODS: The current cross-sectional study was conducted on 404 overweight and obese women. Dietary intake was obtained from FFQ with 147 items. The CAV-1 genotype was measured by the PCR-RFLP method. The anthropometric measurements, serum lipid profile, and inflammatory markers were measured by standard protocols. RESULTS: There was a significant interaction between CAV-1 rs3807992 and healthy DP on high-density cholesterol (HDL) (P-interaction = 0.03), TC/HDL (P-interaction = 0.03) and high sensitivity C-reactive protein (hs-CRP) (P-interaction = 0.04); in A-allele carriers, higher following a healthy DP was related to a higher level of HDL and lower TC/HDL and hs-CRP. As well as, the significant interactions were observed between CAV-1 rs3807992 and unhealthy DP in relation to triglyceride (TG) (P-interaction = 0.001), aspartate aminotransferase (AST) (P-interaction = 0.01) and monocyte chemoattractant protein-1(MCP-1) (P-interaction = 0.01); A-allele carriers were more following the unhealthy DP had lower levels of TG, AST and MCP-1. CONCLUSIONS: Our study revealed a significant gene-diet interaction between rs3807992 SNPs and DPs in relation to cardio-metabolic risk factors; A-allele carriers might be more sensitive to dietary composition compared to GG homozygotes. Following a healthy DP in A-allele-carriers may be improved their genetic association with cardio-metabolic risk factors.

What is the influence of cinnamon supplementation on liver enzymes? A systematic review and meta-analysis of randomized controlled trials.

Existing evidence has uncovered the potential health benefits of cinnamon intake; however, its effect on liver function is unclear. Thus, the aim of this systematic review and meta-analysis was to examine the effect of cinnamon supplementation on liver enzymes. Relevant articles were identified through a systematic search in PubMed/Medline, Scopus, Web of Science, Cochrane Library, and Embase up to September 2020. All trials assessing the effect of oral cinnamon supplementation on serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) in adults were included. The pooled effect sizes were obtained using the random-effects model and expressed as mean difference (MD) and 95% confidence intervals (CI). A total of seven original trials (nine treatment arms) involving a total of 256 subjects were included in the final analysis. The pooled analysis indicated that cinnamon supplementation had no significant effect on serum levels of ALT, AST, and ALP. However, there was a significant reduction in ALT levels in patients with type 2 diabetes (MD: -4.01 U/L; 95% CI: -6.86, -1.15) and in trials with low-dose supplementation (<1,500 mg/d), follow-up duration longer than 12 weeks, and in the elderly patients (aged>50 years). The beneficial effects of cinnamon intake were also shown in AST levels in patients with type 2 diabetes and trials with long-term follow-up (>12 weeks). Longer-term, oral cinnamon supplementation may improve serum levels of liver enzymes in patients with type 2 diabetes. Further high-quality studies are needed, especially in populations with abnormal liver enzyme levels, to firmly establish the clinical efficacy of cinnamon on liver function.

Interaction between Apo A-II -265T>C polymorphism and dietary total antioxidant capacity on some anthropometric indices and serum lipid profile in patients with type 2 diabetes mellitus.

The present study aimed to investigate the interaction of Apo A-II polymorphism and dietary total antioxidant capacity (DTAC) with lipid profile and anthropometric markers in patients with type 2 diabetes (T2DM) that are at risk for atherosclerosis. This cross-sectional study was conducted on 778 patients with T2DM (35-65 years). Dietary intakes were assessed by a 147-item food frequency questionnaire. DTAC was computed using international databases. Participants were categorised into two groups based on rs5082 genotypes. The gene-diet interaction was analysed by an ANCOVA multivariate interaction model. Total cholesterol, TC; triacylglycerol, TG; high- and low-density lipoprotein, HDL and LDL; TC-HDL ratio; waist circumference, WC and body mass index, BMI were obtained according to standard protocols. Overall, the frequency of CC homozygous was 12⋅1 % among study participants. We found that a significant interaction between rs5082 variants and DTAC on mean WC (PTEAC = 0⋅044), TC concentration (PFRAP = 0⋅049 and PTEAC = 0⋅031) and TC/HDL (PFRAP = 0⋅031 and PTRAP = 0⋅040). Among patients whose DTAC was higher than the median intake, the mean of weight, WC and TC/HDL were significantly higher only in individuals with CC genotype. Also, the high DTAC was associated with a lower TC concentration only in T-allele carriers (PFRAP = 0⋅042). We found that adherence to a diet with high total antioxidant capacity can improve the complications of diabetes and atherosclerosis in the T carrier genotype more effectively than the CC genotype. These results could indicate the anti-atherogenic properties of Apo A-II. However, further studies are needed to shed light on this issue.

The effect of vitamin D supplementation on fibroblast growth factor-23 in patients with chronic kidney disease: A systematic review and meta-analysis.

This is a meta-analysis of randomized controlled trials (RCTs) investigating the effects of oral vitamin D supplementation on serum fibroblast growth factor-23 (FGF23) concentrations in patients with chronic kidney disease (CKD). Manuscripts were extracted from PubMed/MEDLINE, Scopus, and ISI Web of Science through February 2020. Subgroup analyses, sensitivity analysis, and meta-regression assessments were performed. A total of eight clinical trials with nine treatment arms were included in the final analysis. The pooled results showed no significant changes in circulating FGF23 following vitamin D supplementation compared to the control group (Standardized mean difference (SMD): 0.24; 95% confidence intervals (CIs): -0.03 to 0.50, p > 0.05). Subgroup analyses found that studies which had participants with a body mass index (BMI) higher than 25 kg/m2 , with an intervention duration shorter than 15 weeks, using phosphate binder medications, and trials that were on both patients with CKD undergoing hemodialysis and patients without hemodialysis treatment produced significant increases in FGF23 when concentration compared with the control group. This meta-analysis provides evidence that vitamin D supplementation does not have a significant effect on plasma FGF23 levels. However, further high-quality trials are required to identify the influence of oral vitamin D supplementation on FGF23 levels in patients with CKD.