scholarly journals The Effectiveness of Myo-Inositol and D-Chiro Inositol Treatment in Type 2 Diabetes

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Basilio Pintaudi ◽  
Giacoma Di Vieste ◽  
Matteo Bonomo
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Side Effects ◽  
Glycemic Control ◽  
Fasting Blood Glucose ◽  
Glucose Lowering ◽  
Insulin Mimetic ◽  
Safe Strategy ◽  
Significant Difference

Inositol has been used as a supplement in treating several pathologies such as PCOS, metabolic syndrome, and gestational diabetes. Both myo-inositol and its isomer d-chiro-inositol showed insulin mimetic effects in conditions of insulin resistance. Type 2 diabetes (T2DM) is a condition typically caused by insulin resistance. There is a lack of evidence of inositol use in T2DM. We evaluated the effectiveness and safety of myo-inositol and d-chiro-inositol treatment in T2DM. This was a pilot study involving a consecutive sample of patients with T2DM with suboptimal glycemic control (HbA1c 7.0–10.0%) already treated with glucose-lowering agents. Patients (23.1% males, mean age of60.8±11.7years) took for three months a combination of myo-inositol (550 mg) and d-chiro-inositol (13.8 mg) orally twice a day as add-on supplement to their glucose-lowering drugs. Possible occurrence of side effects was investigated. After three months of treatment fasting blood glucose (192.6±60.2versus160.9±36.4;p=0.02) and HbA1c levels (8.6±0.9versus7.7±0.9;p=0.02) significantly decreased compared to baseline. There was no significant difference in blood pressure, lipid profile, and BMI levels. None of the participants reported side effects. In conclusion, a supplementation with a combination of myo- and d-chiro-inositol is an effective and safe strategy for improving glycemic control in T2DM.

scholarly journals Relationship of metabolic syndrome defined by IDF or revised NCEP ATP III with glycemic control among Malaysians with Type 2 Diabetes

2020 ◽  
Author(s):  
Riyadh Saif-Ali ◽  
Nor Azmi Kamaruddin ◽  
Molham AL-Habori ◽  
Sami A Al-Dubai ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Glycemic Control ◽  
Medical Center ◽  
Fasting Blood Glucose ◽  
International Diabetes Federation ◽  
C Peptide ◽  
Relationship Of

Abstract Background The chronic complications of Type 2 Diabetes (T2D) such as macrovascular disease is amplified with the increase in the number of metabolic syndrome (MetS) risk factors. This research aims to study the relationship of MetS, diagnosed by the International Diabetes Federation (IDF) or revised National Cholesterol Education Programs Adult Treatment Panel III (NCEP ATP III) criteria, with glycemic control, Fasting blood glucose (FBG), glycated hemoglobin (HbA1c), C-peptide, and insulin resistance in T2D patients.Methods The study is a cross-sectional observational study which, involved 485 T2D patients who are receiving treatment at the University Kebangsaan Malaysia Medical Center (UKMMC), Kuala Lumpur, Malaysia. The MetS among the T2D patients was diagnosed based on IDF and revised NCEP ATP III criteria. C-peptide and HbA1c levels were determined by an automated quantitative immunoassay analyzer and high-performance liquid chromatography, respectively. The MetS factors; FBG, triglyceride, and high-density lipoprotein cholesterol were measured by spectrophotometer. Results Application of the IDF and revised NCEP ATP III criteria respectively resulted in 73% and 85% of the T2D subjects being diagnosed with MetS. The concordance of these criteria in diagnosing MetS among T2D patients was low (κ =0.33, P<0.001). Both IDF and revised NCEP ATP III criteria indicated that T2D patients with 5 MetS factors had higher insulin resistance (P=2.1×10-13;1.4×10-11), C-peptide (P=1.21×10-13; 4.1×10-11), FBG (P=0.01; 0.021), and HbA1c (P=0.039; 0.018) than those T2D patients without MetS, respectively. Conclusion Although there is a low concordance between IDF and revised NCEP ATP III criteria in the diagnosis of MetS among T2D patients, both criteria showed that T2D patients with 5 MetS factors had higher insulin resistance, C-peptide, FBG, and HbA1c.

scholarly journals Insulin resistance limits corneal nerve regeneration in patients with Type 2 diabetes undergoing intensive glycemic control

2021 ◽  
Author(s):  
Georgios Ponirakis ◽  
Muhammad A. Abdul‐Ghani ◽  
Amin Jayyousi ◽  
Mahmoud A. Zirie ◽  
Salma Al‐Mohannadi ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Nerve Regeneration ◽  
Intensive Glycemic Control ◽  
Corneal Nerve

scholarly journals The effects of metformin plus sulfonylurea therapy on clinical features of the metabolic syndrome

2010 ◽  
Vol 63 (9-10) ◽  
pp. 611-615 ◽  
Author(s):  
Branka Koprivica ◽  
Teodora Beljic-Zivkovic ◽  
Tatjana Ille
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Waist Circumference ◽  
Glycemic Control ◽  
Body Mass ◽  
Combined Therapy

Introduction. Insulin resistance is a well-known leading factor in the development of metabolic syndrome. The aim of this study was to evaluate metabolic effects of metformin added to sulfonylurea in unsuccessfully treated type 2 diabetic patients with metabolic syndrome. Material and methods. A group of thirty subjects, with type 2 diabetes, secondary sulfonylurea failure and metabolic syndrome were administered the combined therapy of sulfonylurea plus metformin for six months. Metformin 2000 mg/d was added to previously used sulfonylurea agent in maximum daily dose. Antihypertensive and hypolipemic therapy was not changed. The following parameters were assessed at the beginning and after six months of therapy: glycemic control, body mass index, waist circumference, blood pressure, triglycerides, total cholesterol and its fractions, homeostatic models for evaluation of insulin resistance and secretion (HOMA R, HOMA B) and C- peptide. Results. Glycemic control was significantly improved after six months of the combined therapy: (fasting 7.89 vs. 10.61 mmol/l. p<0.01; postprandial 11.12 vs. 12.61 mmol/l. p<0.01, p<0.01; glycosylated hemoglobin 6.81 vs. 8.83%. p<0.01). the body mass index and waist circumference were significantly lower (26.7 vs. 27.8 kg/m2, p<0.01 and 99.7 vs. 101.4 cm for men, p<0.01; 87.2 vs. 88.5 for women, p<0.01). Fasting plasma triglycerides decreased from 3.37 to 2.45 mmol/l (p<0.001) and HOMA R from 7.04 to 5.23 (p<0.001). No treatment effects were observed on blood pressure, cholesterol, and residual insulin secretion. Conclusion. Administration of metformin in type 2 diabetes with metabolic syndrome decreased cardiovascular risk factors by reducing glycemia, triglycerides, BMI, central obesity and insulin resistance.

Glycemic Control Comparative of Metformin and Glimepiride in Monotherapy of Type 2 Diabetes Mellitus Patient at Islamic Jemursari Hospital Surabaya in 2018

2021 ◽  
Vol 71 (1) ◽  
pp. 24-29
Author(s):  
Rachma Putri Nariswari ◽  
Gwenny Ichsan Prabowo ◽  
Hermina Novida ◽  
Nurina Hasanatuludhhiyah
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Glycemic Control ◽  
Adult Population ◽  
Secondary Data ◽  
Diabetes Mellitus Patient ◽  
Significant Difference ◽  
Tissue Sensitivity

Introduction: Type 2 diabetes mellitus is caused by decreased tissue sensitivity to insulin. The prevalence of diabetes in the world has almost doubled since 1980, from 4.7% to 8.5% in adult population. Early diagnosis and treatment aimed at normalizing glycemic control are very important. The objective of this study was to evaluate and compare glycemic control of metformin and glimepiride in monotherapy of type 2 diabetes mellitus patients at Islamic Jemursari Hospital Surabaya. Method: This was a retrospective observational study using secondary data (medical record), include glycemic control (RPG) before and two months after receiving therapy of outpatients’ type 2 diabetes mellitus with metformin or glimepiride therapy in 2018. 96 samples were found that fit the inclusion criteria. The data were analyzed by Mann-Whitney test. Result: Most patients were female, aged 50-69 years old, and dosage of metformin therapy 1500 mg/day or glimepiride therapy 2 mg/day. There was no significant difference (p>0.05) of glycemic control (RPG) of metformin compared to glimepiride therapies in type 2 diabetes mellitus patients at Islamic Jemursari Hospital Surabaya in 2018. Conclusion: Metformin and glimepiride were not significantly different in glycemic control (RPG). There were patients with RPG >200 mg/dl after two months of metformin or glimepiride therapy.  

scholarly journals Correlation Between Lipid Profile with Type 2 Diabetes Mellitus Progression

2020 ◽  
Vol 8 (2) ◽  
pp. 66-72
Author(s):  
Angiesta Pinakesty ◽  
Restu Noor Azizah
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Glycemic Control ◽  
Lipid Profile ◽  
Cholesterol Levels ◽  
Type 2 Dm ◽  
Hba1c Levels

Introduction: Diabetes mellitus (DM) is a non-communicable disease that has increased from year to year. Type 2 diabetes mellitus is not caused by lack of insulin secretion, but is caused by the failure of the body's cells to respond to the hormone insulin (insulin resistance). Insulin resistance was found to be a major contributor to atherogenic dyslipidemia. Dyslipidemia in DM risks 2 to 4 times higher than non-DM. Although dyslipidemia has a great risk for people with type 2 diabetes mellitus, this conventional risk factor only explains a portion (25%) of excess cardiovascular risk in type 2 DM. Discussion: In uncontrolled type 2 DM patients, LDL oxidation occurs faster which results from an increase in chronic blood glucose levels. Glycemic control as a determinant of DM progressivity is determined through HbA1c examination. HbA1c levels are associated with blood triglyceride levels. Meanwhile, triglyceride levels are associated with total cholesterol and HDL cholesterol levels. HbA1c levels are also associated with LDL cholesterol levels. Conclusion: There is a relationship between lipid profile and the progression of type 2 diabetes mellitus.   Keywords: type 2 diabetes mellitus, dyslipidemia, HbA1c, glycemic control, lipid profile

scholarly journals Triangulating evidence for the causal impact of single-dose zinc supplement on glycemic control for type-2 diabetes

2021 ◽  
Author(s):  
Zhiyang Wang ◽  
Carine Ronsmans ◽  
Benjamin Woolf
Keyword(s):  
Systematic Review ◽  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Glycemic Control ◽  
Fasting Glucose ◽  
Causal Effect ◽  
Fasting Blood Glucose ◽  
Zinc Supplement ◽  
Diabetes Patients

Background: Although previous studies suggested the protective effect of zinc for type-2 diabetes, the unitary causal effect remains inconclusive. Objective: We investigated the causal effect of zinc as a single intervention on glycemic control in type-2 diabetes patients, using a systematic review of RCTs and two-sample Mendelian randomization (MR). Methods: Four outcomes were identified: fasting blood glucose/fasting glucose, hemoglobin A1c (HbA1c), homeostasis model assessment of insulin resistance (HOMA-IR), and serum insulin/fasting insulin level. In the systematic review, four databases were searched up to June 2021. Results were synthesized through the random-effects meta-analysis. Single nucleotide polymorphisms (SNPs) that are independent and are strongly related to zinc supplements were selected from MR-base to perform the two-sample MR with inverse-variance weighted (IVW) coefficient. Results: In the systematic review, 14 trials were included. The zinc supplement led to a significant reduction in the post-trial mean of fasting blood glucose (mean difference (MD): -26.52, 95%CI: -35.13, -17.91), HbA1C (MD: -0.52, 95%CI: -0.90, -0.13), and HOMA-IR (MD: -1.65, 95%CI: -2.62, -0.68), compared to the control group. In the two-sample MR, zinc supplement with 2 SNPs associated with lower fasting glucose (IVW coefficient: -2.04, 95%CI: -3.26, -0.83), but not specified type-2 diabetes. Conclusion: Although the study was limited by the few trials (review) and SNPs (two-sample MR), we demonstrated that the single zinc supplementary improved glycemic control among type-2 diabetes patients with causal evidence to a certain extent.

scholarly journals Intestinal bile acid sequestration improves glucose control by stimulating hepatic miR-182-5p in type 2 diabetes

2018 ◽  
Vol 315 (5) ◽  
pp. G810-G823 ◽  
Author(s):  
Leslie R. Sedgeman ◽  
Carine Beysen ◽  
Ryan M. Allen ◽  
Marisol A. Ramirez Solano ◽  
Scott M. Turner ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Bile Acid ◽  
Glycemic Control ◽  
Mediator Complex ◽  
Glucose Lowering ◽  
Glucose Levels ◽  
Zdf Rats ◽  
Direct Target

Colesevelam is a bile acid sequestrant approved to treat both hyperlipidemia and type 2 diabetes, but the mechanism for its glucose-lowering effects is not fully understood. The aim of this study was to investigate the role of hepatic microRNAs (miRNAs) as regulators of metabolic disease and to investigate the link between the cholesterol and glucose-lowering effects of colesevelam. To quantify the impact of colesevelam treatment in rodent models of diabetes, metabolic studies were performed in Zucker diabetic fatty (ZDF) rats and db/db mice. Colesevelam treatments significantly decreased plasma glucose levels and increased glycolysis in the absence of changes to insulin levels in ZDF rats and db/db mice. High-throughput sequencing and real-time PCR were used to quantify hepatic miRNA and mRNA changes, and the cholesterol-sensitive miR-96/182/183 cluster was found to be significantly increased in livers from ZDF rats treated with colesevelam compared with vehicle controls. Inhibition of miR-182 in vivo attenuated colesevelam-mediated improvements to glycemic control in db/db mice. Hepatic expression of mediator complex subunit 1 (MED1), a nuclear receptor coactivator, was significantly decreased with colesevelam treatments in db/db mice, and MED1 was experimentally validated to be a direct target of miR-96/182/183 in humans and mice. In summary, these results support that colesevelam likely improves glycemic control through hepatic miR-182–5p, a mechanism that directly links cholesterol and glucose metabolism. NEW & NOTEWORTHY Colesevelam lowers systemic glucose levels in Zucker diabetic fatty rats and db/db mice and increases hepatic levels of the sterol response element binding protein 2-responsive microRNA cluster miR-96/182/183. Inhibition of miR-182 in vivo reverses the glucose-lowering effects of colesevelam in db/db mice. Mediator complex subunit 1 (MED1) is a novel, direct target of the miR-96/182/183 cluster in mice and humans.

Increasing endogenous PPARγ ligands improves insulin sensitivity and protects against diet-induced obesity without side effects of thiazolidinediones

2021 ◽  
Author(s):  
Yu-Hua Tseng ◽  
Lee-Ming Chuang ◽  
Yi-Cheng Chang ◽  
Meng-Lun Hsieh ◽  
Lun Tsou ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Side Effects ◽  
Knockout Mice ◽  
Fasting Glucose ◽  
Binding Mode ◽  
Fluid Retention ◽  
Diet Induced Obesity

Abstract Insulin resistance and obesity are pivotal features of type 2 diabetes mellitus. Peroxisome proliferator-activated receptor γ (PPARγ) is a master transcriptional regulator of systemic insulin sensitivity and energy balance. The anti-diabetic drug thiazolidinediones are potent synthetic PPARγ ligands and insulin sensitizers with undesirable side effects including increased adiposity, fluid retention, and osteoporosis, which limit their clinical use. We and others have proved that 15-keto-PGE2 is an endogenous natural PPARγ ligand. 15-keto-PGE2 is catalyzed by prostaglandin reductase 2 (PTGR2) to become inactive metabolites. We found that 15-keto-PGE2 level is increased in Ptgr2 knockout mice. Ptgr2 knockout mice were protected from diet-induced obesity, insulin resistance, and hepatic steatosis without fluid retention nor reduced bone mineral density. Diet-induced obese mice have drastically reduced 15-keto-PGE2 levels compared to lean mice. Administration of 15-keto-PGE2 markedly improved insulin sensitivity and prevented diet-induced obesity in mice. We demonstrated that 15-keto-PGE2 activates PPARγ through covalent binding to its cysteine 285 residue at helix 3, which restrained its binding pocket between helix 3 and β-sheets of the PPARγ ligand binding domain. This binding mode differs from the helix12-dependent binding mode of thiazolidinediones. We further identified a small-molecule PTGR2 inhibitor BPRPT245, which interferes the interaction between the substrate-binding sites of PTGR2 and 15-keto-PGE2. BPRPT245 increased 15-keto-PGE2 concentration, activated PPARγ, and promoted glucose uptake in adipocytes. BPRPT245 also prevented diet-induced obesity, improved insulin sensitivity and glucose tolerance, lowers fasting glucose without fluid retention and osteoporosis. In humans, reduced serum 15-keto-PGE2 levels were observed in patients with type 2 diabetes compared with controls. Furthermore, serum 15-keto-PGE2 levels correlate inversely with insulin resistance and fasting glucose in non-diabetic humans. In conclusion, we identified a new therapeutic approach to improve insulin sensitivity and protect diet-induced obesity through increasing endogenous natural PPARγ ligands without side effects of thiazolidinediones.

scholarly journals Effect of Inulin-Type Carbohydrates on Insulin Resistance in Patients with Type 2 Diabetes and Obesity: A Systematic Review and Meta-Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Mingyue Rao ◽  
Chenlin Gao ◽  
Ling Xu ◽  
Lan Jiang ◽  
Jianhua Zhu ◽  
...  
Keyword(s):  
Systematic Review ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Subgroup Analysis ◽  
Meta Analysis ◽  
The Body ◽  
Obese Patients ◽  
Significant Difference ◽  
Simple Obesity

Background. Insulin resistance (IR) is a physiological condition related to type 2 diabetes mellitus (T2DM) and obesity, which is associated with high blood insulin and glucose. Inulin-type carbohydrate (ITC) is a kind of fermentable fructan that can reduce glucose and ameliorate IR in an animal model, but the effect in clinical trials is controversial. Objective. The authors conducted a systematic literature review to evaluate the effect of ITC supplementation in ameliorating IR in T2DM and obese patients. Methods. Multiple databases were queried for studies before December 25, 2018, which involved supplementation with ITC in ameliorating IR in T2DM and obese patients. Studies that involved meta-analysis of the body mass index (BMI), fasting plasma glucose (FPG), fasting insulin (FI), HbA1c, homeostatic model assessment IR (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) of T2DM subjects were included. HOMA-IR and QUICKI were identified as the primary outcomes. A systematic review was performed to evaluate the effect of ITC on IR in obese patients. Results. The database search yielded 25 studies, which met the inclusion criteria; 11 articles were meta-analyzed, and 5 other articles on T2DM and 9 articles on simple obesity were systematically reviewed. Our results did not find ITC supplementation decrease postintervention and reduction data of BMI (P=0.08). However, it can significantly decrease postintervention and reduction data of FPG, FI, HbA1c, and HOMA-IR. Heterogeneity was eliminated by subgroup analysis according to baseline BMI. There was no significant difference in the amelioration of QUICKI between the ITC and control groups. However, the difference was statistically significant and the heterogeneity was eliminated after subgroup analysis according to intakes of ITC. 14 articles for a systematic review found that the results of blood glucose, insulin, and HbA1c were controversial. Only one of the seven studies on simple obesity concluded that ITC intervention significantly ameliorated HOMA-IR, while the other six did not. Conclusion. Supplementation of ITC can ameliorate IR in T2DM, especially in obese T2DM patients, but the effects are controversial in obese patients.

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