scholarly journals Effects of vitamin K2 supplementation on atherogenic status of individuals with type 2 diabetes: a randomized controlled trial

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Fatemeh Rahimi Sakak ◽  
Nazanin Moslehi ◽  
Hengameh Abdi ◽  
Parvin Mirmiran
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Controlled Trial ◽  
Resistance Index ◽  
Vitamin K2 ◽  
Atherogenic Index ◽  
Oral Glucose ◽  
Double Blind ◽  
Daily Intakes

Abstract Background This study was aimed to examine the effects of vitamin K2 supplementation on atherogenic status, assessed by insulin resistance (IR)-related indexes, in patients with type 2 diabetes mellitus (T2DM). Methods In this double-blind, controlled trial, 68 patients with T2DM on the oral glucose-lowering medications were randomly allocated into two groups receiving daily intakes of 360 μg MK-7 or placebo for 12 weeks. Eight different IR-related indexes were calculated at the baseline and end of the trial. Results At the end of the study, atherogenic coefficient (mean ± SD: − 0.21 ± 0.45 vs. 0.02 ± 0.43; p = 0.043), triglyceride-glucose index (8.88 ± 0.55 vs. 9.23 ± 0.69; p = 0.029), and atherogenic index of plasma (0.37 ± 0.27 vs. 0.51 ± 0.24; p = 0.031) were significantly lower in the vitamin K2 group, compared to the placebo. However, after accounting for their baseline values, the differences were no more significant. No significant differences were observed in Castelli’s Ӏ and ӀӀ risk indexes, the ratio of triglycerides to high-density lipoprotein cholesterol, lipoprotein combine index, and the metabolic score for insulin resistance index between the two groups at the end of the study. Conclusions Daily intakes of 360 μg vitamin K2 in the form of MK-7 for 12 weeks could not improve the IR-related indexes of Cardiovascular Diseases risk. Trial registration The trial was registered on Iranian Registry of Clinical Trials registry (Trial ID. IRCT20190824044592N1) on 22 December 2019. The record can be found at https://en.irct.ir/trial/41728.

scholarly journals The Ideal Insulin Resistance Index for c\Cardiovascular Risk Discrimination in type 2 Diabetes Mellitus

2021 ◽  
Author(s):  
Taoreed Adegoke Azeez
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Risk ◽  
Resistance Index ◽  
Atherogenic Index ◽  
High Cardiovascular Risk ◽  
Insulin Resistance Index ◽  
Fasting Plasma ◽  
The Mean

Abstract BackgroundThis study was aimed at determining the correlation between insulin resistance indices and atherogenic index as well as determining the ability of the indices to discriminate between low and high cardiovascular risk in diabetic individuals. The study involved 70 participants. Ethical approval was granted by the institution review board. Fasting plasma glucose, insulin and lipid profile were analyzed for each participant. Atherogenic index of plasma (AIP), homeostatic mode assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), fasting glucose insulin ratio (FGIR), fasting insulin resistance index (FIRI), McAuley’s index and Raynauld’s index were calculated using the appropriate formulae. Pearson’s correlation and receiver operating characteristic (ROC) analysis were done.ResultsThe mean age of the participants was 53.34 ± 9.57 years. Males were 50%. The mean duration of type 2 diabetes in the participants was 6.29 ± 2.78 years. Each index had a strong and significant correlation with fasting plasma insulin (p<0.001). Using AIP as a marker of cardiovascular risk, 14.3% had intermediate/high risk. Among the indices, only McAuley’s index showed a statistically significant negative correlation with AIP (r= -0.453;p<0.001). None of the indices could reliably discriminate between low and intermediate/high cardiovascular risk.ConclusionThe studied indices could not predict cardiovascular risk despite their usefulness as insulin resistance markers. Further studies are needed to identify an ideal insulin resistance index that can also predict cardiovascular risk.

scholarly journals Effect of chronic liraglutide therapy and its withdrawal on time to postchallenge peak glucose in type 2 diabetes

2018 ◽  
Vol 314 (3) ◽  
pp. E287-E295 ◽  
Author(s):  
Susan Tran ◽  
Caroline K. Kramer ◽  
Bernard Zinman ◽  
Haysook Choi ◽  
Ravi Retnakaran
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Controlled Trial ◽  
Oral Glucose ◽  
Β Cell ◽  
Double Blind ◽  
Time To Peak ◽  
Β Cell Function

Delayed timing of peak serum glucose following an oral glucose challenge can predict declining β-cell function and worsening glucose tolerance over time. Accordingly, postchallenge peak glucose is typically delayed in patients with type 2 diabetes (T2DM). However, little is known about the capacity of antidiabetic medications to reverse this delay. Thus, we sought to evaluate the effect of the glucagon-like peptide-1 agonist liraglutide on time to peak glucose in early T2DM. In this secondary analysis of a double-blind placebo-controlled trial, 51 patients with T2DM of 2.6 ± 1.9 yr duration were randomized to daily subcutaneous liraglutide or placebo injection for 48 wk, with oral glucose tolerance test (OGTT) performed every 12 wk while on therapy and after a 2-wk washout. On each OGTT, time to peak glucose was determined from venous glucose measurements at 0, 10, 20, 30, 60, 90, and 120 min. At randomization, most patients in both arms exhibited peak glucose at 90 min postchallenge. By 12 wk, 65.4% of the liraglutide arm had shifted to an earlier peak (vs. 36% on placebo; P = 0.19), with little change thereafter at 24, 36, and 48 wk. After the 2-wk washout, however, 57.7% of those who had been on liraglutide reverted to a later peak (vs. 4.5% on placebo; P < 0.001). This shift was associated with declining β-cell function ( P = 0.001), resulting in higher 2-h blood glucose at washout in the liraglutide arm compared with placebo ( P = 0.001). Thus, although liraglutide possibly might improve the delay in peak glucose, its cessation yielded a worsening thereof and higher glycemia. The mechanisms underlying these observations and their clinical implications warrant further investigation.

scholarly journals Changes in insulin sensitivity during leptin replacement therapy in leptin-deficient patients

2008 ◽  
Vol 295 (6) ◽  
pp. E1401-E1408 ◽  
Author(s):  
Gilberto Paz-Filho ◽  
Karin Esposito ◽  
Barry Hurwitz ◽  
Anil Sharma ◽  
Chuanhui Dong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Mixed Model ◽  
Resistance Index ◽  
Oral Glucose ◽  
Model Assessment ◽  
Rapid Weight Gain ◽  
Hypoglycemic Reaction ◽  
Homeostatic Model Assessment

Leptin replacement rescues the phenotype of morbid obesity and hypogonadism in leptin-deficient adults. However, leptin's effects on insulin resistance are not well understood. Our objective was to evaluate the effects of leptin on insulin resistance. Three leptin-deficient adults (male, 32 yr old, BMI 23.5 kg/m2; female, 42 yr old, BMI 25.1 kg/m2; female, 46 yr old, BMI 31.7 kg/m2) with a missense mutation of the leptin gene were evaluated during treatment with recombinant methionyl human leptin (r-metHuLeptin). Insulin resistance was determined by euglycemic hyperinsulinemic clamps and by oral glucose tolerance tests (OGTTs), whereas patients were on r-metHuLeptin and after treatment was interrupted for 2–4 wk in the 4th, 5th, and 6th years of treatment. At baseline, all patients had normal insulin levels, C-peptide, and homeostatic model assessment of insulin resistance index, except for one female diagnosed with type 2 diabetes. The glucose infusion rate was significantly lower with r-metHuLeptin (12.03 ± 3.27 vs. 8.16 ± 2.77 mg·kg−1·min−1, P = 0.0016) but did not differ in the 4th, 5th, and 6th years of treatment when all results were analyzed by a mixed model [ F( 1 , 4 ) = 0.57 and P = 0.5951]. The female patient with type 2 diabetes became euglycemic after treatment with r-metHuLeptin and subsequent weight loss. The OGTT suggested that two patients showed decreased insulin resistance while off treatment. During an off-leptin OGTT, one of the patients developed a moderate hypoglycemic reaction attributed to increased posthepatic insulin delivery and sensitivity. We conclude that, in leptin-deficient adults, the interruption of r-metHuLeptin decreases insulin resistance in the context of rapid weight gain. Our results suggest that hyperleptinemia may contribute to mediate the increased insulin resistance of obesity.

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