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The Effects of Synbiotic Supplementation on Glucose Metabolism and Lipid Profiles in Patients with Diabetes: a Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Tabrizi R
,Moosazadeh M
,Lankarani KB
,Akbari M
,Heydari ST
,Kolahdooz F
,Asemi Z
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The Effects of Vitamin D Supplementation on Glucose Metabolism and Lipid Profiles in Patients with Gestational Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
This systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to summarize the effect of vitamin D supplementation on glucose homeostasis parameters and lipid profiles in gestational diabetes (GDM) patients. We conducted an electronic systematic search of MEDLINE, and 4 other research databases from inception to August 2016, in addition to performing hand searches and consulting with experts in the field. The index of heterogeneity between studies was determined using Cochran (Q) and I-squared tests. Given the existing heterogeneity between studies, a fix or random effect model was performed to estimate the standardized mean difference (SMD) for each variable by using inverse variance method and Cohen statistics. Six randomized clinical trials (187 subjects and 184 controls) were included. The results showed that vitamin D supplementation significantly reduced the homeostasis model assessment of insulin resistance (HOMA-IR) [SMD -0.66; 95% confidence interval (CI), -1.14 to -0.18], homeostatic model assessment-B cell function (HOMA-B) (SMD -0.52; 95% CI, -0.79 to -0.25), LDL-cholesterol levels (SMD -0.33; 95% CI, -0.58 to -0.07), and significantly increased quantitative insulin sensitivity check index (QUICKI) (SMD 0.73; 95% CI, 0.26 to 1.20). We found no beneficial effect of vitamin D supplementation on fasting plasma glucose (FPG), insulin, HbA1c, total-, HDL-cholesterol, and triglycerides concentrations. In conclusion, this meta-analysis demonstrated that vitamin D supplementation may lead to an improvement in HOMA-IR, QUICKI, and LDL-cholesterol levels, but did not affect FPG, insulin, HbA1c, triglycerides, total- and HDL-cholesterol levels; however, vitamin D supplementation increased HOMA-B.
Akbari M
,Moosazaheh M
,Lankarani KB
,Tabrizi R
,Samimi M
,Karamali M
,Jamilian M
,Kolahdooz F
,Asemi Z
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The Effects of Selenium Supplementation on Glucose Metabolism and Lipid Profiles Among Patients with Metabolic Diseases: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
This systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to summarize the effect of selenium administration on glucose metabolism and lipid profiles among patients with diseases related to metabolic syndrome (MetS). We searched the following databases up to May 2017: MEDLINE, EMBASE, Web of Science, and Cochrane Central Register of Controlled Trials. The relevant data were extracted and assessed for quality of the studies according to the Cochrane risk of bias tool. Data were pooled using the inverse variance method and expressed as standardized mean difference (MDs) with 95% confidence intervals (95% CI). Five studies were included in the meta-analyses. The results showed that selenium supplementation significantly reduced insulin levels (SMD -0.42; 95% CI, -0.83 to -0.01) and increased quantitative insulin sensitivity check index (QUICKI) (SMD 0.83; 95% CI, 0.58 to 1.09). Selenium supplementation had no beneficial effects on other glucose homeostasis parameters, such as fasting plasma glucose (FPG) (SMD -0.29; 95% CI, -0.73 to 0.15), homeostasis model assessment of insulin resistance (HOMA-IR) (SMD -0.80; 95% CI, -1.58 to -0.03), and lipid profiles, such as triglycerides (SMD -0.42; 95% CI, -0.83 to -0.01), VLDL- (SMD -0.42; 95% CI, -0.83 to -0.01), total- (SMD -0.42; 95% CI, -0.83 to -0.01), LDL- (SMD 0.02; 95% CI, -0.20 to 0.24), and HDL-cholesterol (SMD 0.16; 95% CI, -0.06 to -0.38). Overall, this meta-analysis showed that selenium administration may lead to an improvement in insulin and QUICKI, but did not affect FPG, HOMA-IR, and lipid profiles.
Tabrizi R
,Akbari M
,Moosazadeh M
,Lankarani KB
,Heydari ST
,Kolahdooz F
,Mohammadi AA
,Shabani A
,Badehnoosh B
,Jamilian M
,Assarian A
,Asemi Z
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The effects of alpha-lipoic acid supplementation on glucose control and lipid profiles among patients with metabolic diseases: A systematic review and meta-analysis of randomized controlled trials.
This systematic review and meta-analysis of randomized controlled trials (RCTs) was performed to summarize the effect of alpha-lipoic acid (ALA) supplementation on glycemic control and lipid profiles among patients with metabolic diseases.
We searched the following databases till October 2017: MEDLINE, EMBASE, Web of Science and Cochrane Central Register of Controlled Trials. The relevant data were extracted and assessed for quality of the studies according to the Cochrane risk of bias tool. Data were pooled using the inverse variance method and expressed as standardized mean difference (SMD) with 95% confidence intervals (95% CI). Heterogeneity between studies was assessed by the Cochran Q statistic and I-squared tests (I2). Twenty-four studies were included in the meta-analyses.
The findings of this meta-analysis showed that ALA supplementation among patients with metabolic diseases significantly decreased fasting glucose (SMD -0.54; 95% CI, -0.89, -0.19; P = 0.003), insulin (SMD -1.01; 95% CI, -1.70, -0.31; P = 0.006), homeostasis model assessment of insulin resistance (SMD -0.76; 95% CI, -1.15, -0.36; P < 0.001) and hemoglobin A1c (SMD -1.22; 95% CI, -2.01, -0.44; P = 0.002), triglycerides (SMD -0.58; 95% CI, -1.00, -0.16; P = 0.006), total- (SMD -0.64; 95% CI, -1.01, -0.27; P = 0.001), low density lipoprotein-cholesterol (SMD -0.44; 95% CI, -0.76, -0.11; P = 0.008). We found no detrimental effect of ALA supplementation on high density lipoprotein-cholesterol (HDL-cholesterol) levels (SMD 0.57; 95% CI, -0.14, 1.29; P = 0.11).
Overall, the current meta-analysis demonstrated that ALA administration may lead to an improvement in glucose homeostasis parameters and lipid profiles except HDL-cholesterol levels.
Akbari M
,Ostadmohammadi V
,Lankarani KB
,Tabrizi R
,Kolahdooz F
,Khatibi SR
,Asemi Z
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The effects of folate supplementation on lipid profiles among patients with metabolic diseases: A systematic review and meta-analysis of randomized controlled trials.
Although several studies have assessed the effect of folate supplementation on lipid profiles among patients with metabolic diseases, findings are inconsistent. This review of randomized controlled trials (RCTs) was conducted to summarize the evidence on the effects of folate supplementation on lipid profiles among patients with metabolic diseases.
Randomized-controlled trials (RCTs) published in PubMed, EMBASE, Web of Science and Cochrane Library databases up to until 20 August 2017 were searched. Two review authors independently assessed study eligibility, extracted data, and evaluated risk of bias of included studies. Heterogeneity was measured with a Q-test and with I2 statistics. Data were pooled by using the fix or random-effect model based on the heterogeneity test results and expressed as standardized mean difference (SMD) with 95% confidence interval (CI).
A total of thirteen randomized controlled trials were included. Folate supplementation did not affect systolic blood pressure (SMD -0.87; 95% CI, -1.83, 0.09) and diastolic blood pressure (SMD -0.59; 95% CI, -1.55, 0.37), and lipid profiles including triglycerides (SMD 0.10; 95% CI, -0.42, 0.63), total- (SMD 0.06; 95% CI, -0.31, 0.43), HDL- (SMD 0.04; 95% CI, -0.36, 0.44), VLDL- (SMD 0.08; 95% CI, -0.24, 0.41), and LDL-cholesterol (SMD -0.14; 95% CI, -0.55, 0.28).
Folate supplementation did not affect blood pressures and lipid profiles among patients with metabolic diseases. Additional prospective studies regarding the impact of folate supplementation on blood pressures and lipid profiles in patients with metabolic diseases are necessary.
Tabrizi R
,Lankarani KB
,Akbari M
,Naghibzadeh-Tahami A
,Alizadeh H
,Honarvar B
,Sharifi N
,Mazoochi M
,Ostadmohammadi V
,Fatholahpour A
,Asemi Z
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