Insulin Resistance Impairs Cognitive Performance Even in Healthy Subjects at Risk for Diabetes Mellitus

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1830-P ◽  
Author(s):  
GIAN PIO SORICE ◽  
ILARIA IMPROTA ◽  
TERESA MEZZA ◽  
SARA GRIONI ◽  
GIOVANNA MASONE IACOBUCCI ◽  
...  
2019 ◽  
Vol 11 (04) ◽  
pp. 317-322
Author(s):  
Hayder M. Al-Kuraishy ◽  
Ali I. Al-Gareeb ◽  
Hala A. Shams ◽  
Farah Al-Mamorri

Abstract OBJECTIVES: The objective of the study was to evaluate the effect of metformin alone or in combination with coenzyme Q10 (CoQ10) on inflammatory changes and endothelial dysfunction in patients with type 2 diabetes mellitus (T2DM). MATERIALS AND METHODS: A total numbers of 54 patients with T2DM compared to 30 healthy subjects were divided into three groups: Group A (n = 30): healthy subjects without any medications; Group B (n = 24): T2DM patients treated with metformin 1 g/day; and Group C (n = 30): T2DM patients treated with metformin 1 g/day plus CoQ10, 300 mg/day. The duration of the study was 8 weeks. Fasting blood glucose, glycated hemoglobin, lipid profile, blood pressure variables, fasting insulin, insulin resistance, homeostatic model assessment of insulin resistance, vascular cell adhesion molecule 1 (VCAM-1), and E-selectin were measured before and after therapy. RESULTS: Metformin and/or CoQ10 therapy illustrated an insignificant effect on the fody mass index. This combination produced a significant improvement of metabolic changes in patients with T2DM (P < 0.01). sVCAM-1 serum level was decreased significantly after the initiation of metformin and/or CoQ10 therapy compared to the baseline P < 0.05. E-selectin was declined significantly following metformin monotherapy and after metformin plus CoQ10 therapy (P = 0.0001). CONCLUSION: CoQ10 add-on metformin therapy improves endothelial dysfunction and inflammatory changes in patients with T2DM alongside with amelioration of metabolic profile.


2015 ◽  
Vol 2 ◽  
pp. 2333794X1456845 ◽  
Author(s):  
Soulmaz Fazeli Farsani ◽  
Marloes P. van der Aa ◽  
Catherijne A. J. Knibbe ◽  
Anthonius de Boer ◽  
Marja M. J. van der Vorst

Objectives. To evaluate body mass index standard deviation score (BMI-SDS), insulin sensitivity, and progression to type 2 diabetes mellitus (T2DM) in children at risk for T2DM approximately 3 years after being diagnosed with overweight/obesity and insulin resistance (measured by Homeostasis Model Assessment of Insulin Resistance [HOMA-IR]). Methods. Out of 86 invited children, 44 (mean age 15.4 ± 3.6 years) participated. Medical history, physical examination, and laboratory workup were performed. Results. While the mean BMI-SDS significantly increased from 2.9 to 3.4, the mean HOMA-IR significantly decreased from 5.5 to 4.6 (baseline vs follow-up visit). Change in HOMA-IR was only due to a decrease in mean fasting plasma insulin (24.1 vs 21.1, P = .073). Conclusions. Although increase in BMI-SDS in these children is worrisome, the American Diabetes Association recommended screening interval of 3 years for children at risk for T2DM is not too long based on the fact that none of our study participants developed T2DM.


2011 ◽  
Vol 96 (2) ◽  
pp. 447-453 ◽  
Author(s):  
Katrine B. Hansen ◽  
Tina Vilsbøll ◽  
Jonatan I. Bagger ◽  
Jens J. Holst ◽  
Filip K. Knop

abstract Objective: Increased postprandial glucose-dependent insulinotropic polypeptide (GIP) and glucagon responses and reduced postprandial glucagon-like peptide-1 (GLP-1) responses have been observed in some patients with type 2 diabetes mellitus. The causality of these pathophysiological traits is unknown. We aimed to determine the impact of insulin resistance and reduced glucose tolerance on postprandial GIP, GLP-1, and glucagon responses in healthy subjects. Research Design and Methods: A 4-h 2200 KJ-liquid meal test was performed in 10 healthy Caucasian males without family history of diabetes [age, 24 ± 3 yr (mean ± sd); body mass index, 24 ± 2 kg/m2; fasting plasma glucose, 4.9 ± 0.3 mm; hemoglobin A1c, 5.4 ± 0.1%] before and after intervention using high-calorie diet, relative physical inactivity, and administration of prednisolone (37.5 mg/d) for 12 d. Results: The intervention resulted in insulin resistance according to the homeostatic model assessment [1.1 ± 0.3 vs. 2.3 (mean ± sem) ± 1.3; P = 0.02] and increased postprandial glucose excursions [area under curve (AUC), 51 ± 28 vs. 161 ± 32 mm · 4 h; P = 0.045], fasting plasma insulin (36 ± 3 vs. 61 ± 6 pm; P = 0.02), and postprandial insulin responses (AUC, 22 ± 6 vs. 43 ± 13 nm · 4 h; P = 0.03). This disruption of glucose homeostasis had no impact on postprandial GLP-1 responses (AUC, 1.5 ± 0.7 vs. 2.0 ± 0.5 nm · 4 h; P = 0.56), but resulted in exaggerated postprandial GIP (6.2 ± 1.0 vs. 10.0 ± 1.3 nm · 4 h; P = 0.003) and glucagon responses (1.6 ± 1.5 vs. 2.4 ± 3.2; P = 0.007). Conclusions: These data suggest that increased postprandial GIP and glucagon responses may occur as a consequence of insulin resistance and/or reduced glucose tolerance. Our data suggest that acute disruption of glucose homeostasis does not result in reduced postprandial GLP-1 responses as observed in some individuals with type 2 diabetes mellitus.


2011 ◽  
Vol 58 (2) ◽  
pp. 173-180 ◽  
Author(s):  
Anne K Monroe ◽  
Adrian S Dobs ◽  
Xiaoqiang Xu ◽  
Frank J Palella ◽  
Lawrence A Kingsley ◽  
...  

2020 ◽  
Author(s):  
Hossein Chiti ◽  
Mohammad Hossein Izadi ◽  
Saeideh Mazloomzadeh

Insulin resistance in gestational diabetes increases maternal and fetal complications. Tumor necrosis factor-alpha (TNF-α) is an inflammatory factor associated with insulin resistance. The aim of this study was to determine the association between pregnancy serum TNF-α level and postpartum insulin resistance in patients with gestational diabetes mellitus. 50 pregnant women, including 25 cases of gestational diabetes and 25 healthy pregnant women, were evaluated. First, during the third trimester of pregnancy, serum TNF-α level of all cases were measured. Two months after delivery, based on the obtained results from insulin levels and a 2-hour glucose tolerance test, HOMA-IR and HOMA-B were calculated, and the association between serum TNF-α level and insulin resistance was determined. Data were analyzed using independent t-test, Mann-Whitney, and chi-square test in SPSS software. The mean serum level of TNF-α in women with gestational diabetes mellitus was higher than healthy subjects, but there was no significant difference between the two groups. The serum level of insulin, HOMA-IR and HOMA-B indices in women with gestational diabetes mellitus were higher than healthy subjects, with a significant difference in all of the measures between two groups (P=0.0001). There was no significant correlation between TNF-α and HOMAIR levels in insulin-resistant mothers two months after delivery (r=−0.33). Also, no significant correlation was detected between pregnancy TNF-α levels and HOMA-B index. Despite the higher serum levels of insulin, HOMA-IR, and HOMA-B in the diabetic group, the serum TNF-α level did not show any correlation with insulin resistance after delivery.


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