scholarly journals The Type 2 Deiodinase Thr92Ala Polymorphism Is Associated with Higher Body Mass Index and Fasting Glucose Levels: A Systematic Review and Meta-Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xichang Wang ◽  
Kan Chen ◽  
Chenyu Zhang ◽  
Haoyu Wang ◽  
Jiashu Li ◽  
...  

Background. Type 2 deiodinase (Dio2) is a selenoenzyme that is mainly expressed in the endoplasmic reticulum of the central nervous system, brown adipose tissue, and placenta and is responsible for outer ring deiodination of thyroxine (T4) to form biologically active triiodothyronine (T3). The Thr92Ala polymorphism of Dio2 has been found to be a potential risk factor for various diseases beyond the hypothalamus-pituitary-thyroid (HPT) axis. Methods. We searched the relevant studies in the PubMed, Embase, and Cochrane Library databases and Google Scholar. A systematic review and meta-analysis of studies on the Thr92Ala polymorphism and metabolic parameters beyond the HPT axis (e.g., BMI, fasting glycemic traits, plasma lipid levels, and hypertension risk) were performed. Results. Six eligible studies that analyzed the relationship between the Thr92Ala polymorphism and metabolic parameters beyond the thyroid were identified. All selected studies excluded patients with thyroid dysfunction, and diabetic patients were also excluded when fasting glucose and fasting insulin levels were meta-analyzed. The Thr92Ala polymorphism was found to be a significant risk factor for higher BMI (Std. mean difference 0.31 (0.01, 0.60), p = 0.04 ) and higher fasting glucose levels (Std. mean difference 1.18 (0.05, 2.31), p = 0.04 ). However, fasting insulin levels, plasma lipid levels, and hypertension risk showed a nonsignificant association with the Thr92Ala polymorphism. Conclusion. Compared with euthyroid noncarriers (Thr/Thr), euthyroid Ala92-Dio2 carriers showed increased BMI levels, and Ala92-Dio2 carriers also had higher fasting plasma glucose levels than matched euthyroid nondiabetic noncarriers.

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Ilse C Schrieks ◽  
Annelijn L Heil ◽  
Henk F Hendriks ◽  
Kenneth J Mukamal ◽  
Joline W Beulens

Introduction: Moderate alcohol consumption is associated with a reduced risk of type 2 diabetes, but this relation appears stronger for women than men. The reduced risk of diabetes could be explained by improved insulin sensitivity or glycemic status, but results of intervention studies on this relation are inconsistent. Our aim was to conduct a systematic review and meta-analysis of intervention studies investigating the effect of alcohol consumption on insulin sensitivity and glycemic status. Design: Systematic review and meta-analysis of intervention studies. Data sources: PubMed and Embase were searched until May 2013 using a pre-specified search string. Methods: Intervention studies on the effect of more than 2 weeks alcohol consumption on biological markers of insulin sensitivity or glycemic status were identified and assessed on their quality. Pooled standardized mean differences (SMD) were calculated using either fixed or random effects models. Gender-stratified analyses and sensitivity analyses excluding studies with high doses of alcohol (> 40 g/day). In a meta-regression the influence of dosage and duration of intervention was tested. Results: We included 14 intervention studies in a meta-analysis on 6 glycemic endpoints. Alcohol consumption did not influence insulin sensitivity (SMD=0.06 [-0.13 to 0.26]) or fasting glucose (SMD=0.09 [-0.09 to 0.27]). Alcohol consumption reduced HbA1c (SMD=-0.62 [-1.01 to -0.23], P=0.002) and insulin concentrations (SMD=-0.17 [-0.34 to 0.00] P=0.049) compared with the control group. In women, alcohol consumption reduced fasting insulin (SMD=-0.23 [-0.41 to -0.04], P=0.019) and improved insulin sensitivity (SMD=0.19 [-0.03 to 0.41], P=0.087), but no significant differences were observed among men. Results were similar when only studies with moderate alcohol dosages were analysed and were not influenced by dosage and duration of the intervention. Conclusions: This study showed that moderate alcohol consumption may reduce fasting insulin and improve insulin sensitivity among women, but not among men. These effects may provide an explanation for the relation between alcohol consumption and type 2 diabetes. Furthermore, moderate alcohol consumption may reduce HbA1c levels among both men and women.


2015 ◽  
Author(s):  
Qian Wang ◽  
Andrew Grainger ◽  
Ani Manichaikul ◽  
Emily Farber ◽  
Suna Onengut-Gumuscu ◽  
...  

Individuals with dyslipidemia often develop type 2 diabetes, and diabetic patients often have dyslipidemia. It remains to be determined whether there are genetic connections between the 2 disorders. A female F2 cohort, generated from BALB/cJ (BALB) and SM/J (SM) Apoe-deficient (Apoe−/−) strains, was fed a Western diet for 12 weeks. Fasting plasma glucose and lipid levels were measured before and after Western diet feeding. 144 genetic markers across the entire genome were used for analysis. One significant QTL on chromosome 9, named Bglu17 [26.4 cM, logarithm of odds ratio (LOD): 5.4], and 3 suggestive QTLs were identified for fasting glucose levels. The suggestive QTL near the proximal end of chromosome 9 (2.4 cM, LOD: 3.12) was detected when mice were fed chow or Western diet and named Bglu16. Bglu17 coincided with a significant QTL for HDL and a suggestive QTL for non-HDL cholesterol levels. Plasma glucose levels were inversely correlated with HDL but positively correlated with non-HDL cholesterol levels in F2 mice fed either diet. A significant correlation between fasting glucose and triglyceride levels was observed on the Western but not chow diet. Haplotype analysis revealed that ???lipid genes??? Sik3 and Apoc3 were probable candidates for Bglu17. We have identified multiple QTLs for fasting glucose and lipid levels. The colocalization of QTLs for both phenotypes and the sharing of potential causal genes suggest that dyslipidemia and type 2 diabetes are genetically connected.


2020 ◽  
Vol 112 (4) ◽  
pp. 1002-1014 ◽  
Author(s):  
Arno Greyling ◽  
Katherine M Appleton ◽  
Anne Raben ◽  
David J Mela

ABSTRACT Background It has been suggested that low-energy sweeteners (LES) may be associated with an increased risk of metabolic diseases, possibly due to stimulation of glucose-responsive mechanisms. Objective We conducted a systematic review and meta-analysis of human intervention studies examining the acute effect of LES intake on postprandial glucose (PPG) and postprandial insulin (PPI) responses, in order to comprehensively and objectively quantify these relations. Methods We systematically searched the Medline, OVID FSTA, and SCOPUS databases until January 2020. Randomized controlled trials comparing acute postprandial effects on PPG and/or PPI after exposure to LES, either alone, with a meal, or with other nutrient-containing preloads to the same intervention without LES were eligible for inclusion. PPG and PPI responses were calculated as mean incremental area under the curve divided by time. Meta-analyses were performed using random effects models with inverse variance weighing. Results Twenty-six papers (34 PPG trials and 29 PPI trials) were included. There were no reports of statistically significant differences in the effects of LES on PPG and PPI responses compared with control interventions. Pooled effects of LES intake on the mean change difference in PPG and PPI were −0.02 mmol/L (95% CI: −0.09, 0.05) and −2.39 pmol/L (95% CI: −11.83, 7.05), respectively. The results did not appreciably differ by the type or dose of LES consumed, cointervention type, or fasting glucose and insulin levels. Among patients with type 2 diabetes, the mean change difference indicated a smaller PPG response after exposure to LES compared with the control (−0.3 mmol/L; 95% CI: −0.53, −0.07). Conclusions Ingestion of LES, administered alone or in combination with a nutrient-containing preload, has no acute effects on the mean change in postprandial glycemic or insulinemic responses compared with a control intervention. Apart from a small beneficial effect on PPG (−0.3 mmol/L) in studies enrolling patients with type 2 diabetes, the effects did not differ by type or dose of LES, or fasting glucose or insulin levels. This review and meta-analysis was registered at PROSPERO as CRD42018099608.


2017 ◽  
Vol 176 (1) ◽  
pp. R1-R14 ◽  
Author(s):  
Yvonne H M Krul-Poel ◽  
Marieke M ter Wee ◽  
Paul Lips ◽  
Suat Simsek

Objective Epidemiologic studies suggest that vitamin D status plays a role in glycaemic control in patients with type 2 diabetes. However, intervention studies yielded inconsistent results. The aim of this study is to systematically review the effect of vitamin D supplementation on glycaemic control in patients with type 2 diabetes. Methods Systematic review and meta-analysis. We searched Medline, Embase and the Cochrane Library for RCTs examining the effect of vitamin D supplementation on glycaemic control in patients with type 2 diabetes. A random-effects model meta-analysis was performed to obtain a summarized outcome of vitamin D supplementation on HbA1c, fasting glucose and homeostasis model assessment – insulin resistance (HOMA-IR). Results Twenty-three RCTs were included in this systematic review representing a total of 1797 patients with type 2 diabetes. Mean (± s.d.) change in serum 25-hydroxyvitamin D varied from 1.8 ± 10.2 nmol/L to 80.1 ± 54.0 nmol/L. Nineteen studies included HbA1c as outcome variable. Combining these studies no significant effect in change of HbA1c was seen after vitamin D intervention compared with placebo. A significant effect of vitamin D supplementation was seen on fasting glucose in a subgroup of studies (n = 4) with a mean baseline HbA1c ≥ 8% (64 mmol/mol) (standardized difference in means: 0.36; 95% CI: 0.12–0.61, P = 0.003). Conclusions Current evidence of RCTs does not support short-term vitamin D supplementation in a heterogeneous population with type 2 diabetes. However, in patients with poorly controlled diabetes, a favourable effect of vitamin D is seen on fasting glucose.


Obesity ◽  
2018 ◽  
Vol 27 (1) ◽  
pp. 94-102 ◽  
Author(s):  
Hang Zhao ◽  
An Song ◽  
Yunjia Zhang ◽  
Linyi Shu ◽  
Guangyao Song ◽  
...  

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