scholarly journals Prevalence of Abnormal Glucose Metabolism and Insulin Resistance Among Subtypes of Ischemic Stroke in Japanese Patients

Stroke ◽  
2009 ◽  
Vol 40 (4) ◽  
pp. 1289-1295 ◽  
Author(s):  
Takao Urabe ◽  
Hirotaka Watada ◽  
Yasuyuki Okuma ◽  
Ryota Tanaka ◽  
Yuji Ueno ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Ischemic Stroke ◽  
Glucose Metabolism ◽  
Japanese Patients ◽  
Abnormal Glucose Metabolism

Abstract TP416: Effects Of Pioglitazone In Patients With Abnormal Glucose Metabolism After Stroke The J-SPIRIT Study

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Ryota Tanaka ◽  
Kazuo Yamashiro ◽  
Yasutaka Tanaka ◽  
Nobukazu Miyamoto ◽  
Yuji Ueno ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Ischemic Stroke ◽  
Glucose Metabolism ◽  
Recurrent Stroke ◽  
Controlled Trial ◽  
Control Group ◽  
Placebo Control ◽  
Newly Diagnosed ◽  
Abnormal Glucose Metabolism ◽  
Multicenter Randomized Controlled Trial

Background and aims: The stroke patients with abnormal glucose metabolism are increasing in Japan. The J-SPIRIT study (Juntendo the Stroke Prevention study in Insulin Resistance and Impaired glucose Tolerance) was planned to investigate the effect of pioglitazone on the reduction of recurrent stroke in the patients with abnormal glucose metabolism and insulin resistance after ischemic stroke. Methods: The study is a multicenter, randomized controlled trial performed in the four hospitals in Tokyo or neighboring cities in Japan. We enrolled the patients who ; (1) were 35 to 85 years old ; (2) had symptomatic ischemic stroke; (3) had no history of diabetes and no evidence of diabetes by initial blood test. Among those patients, a standard OGTT with 75g of glucose was performed at least 2 weeks after admission. We enrolled the patients of newly diagnosed diabetes and IGT by OGTT, and randomized these patients to receive either pioglitazone or matching placebo. Results: Total 134 patients were enrolled. 58 patients were received pioglitazone, 61 were placebo control. Mean HbA1c were not different among both groups (5.6±0.38 pioglitazone vs 5.5±0.38 control) and mean observation period were 25±19.9 months in piolgitazone group and 30±16 months in control group. The data showed a trend of benefit with pioglitazone for the primary end point of recurrence of ischemic stroke compared to placebo control. (event rate=3.4% pioglitazone vs 11.6% control) Conclusions: Our data indicated pioglitazone might be able reduce the risk of recurrent stroke in the patients of ischemic stroke with newly diagnosed abnormal glucose metabolism and insulin resistance.

O-163 Hyperandrogenaemia in early adulthood is an independent risk factor for abnormal glucose metabolism in later life

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
K Tuorila ◽  
M M Ollila ◽  
M R Järvelin ◽  
J Tapanainen ◽  
S Franks ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Fasting Glucose ◽  
Early Adulthood ◽  
Positive Association ◽  
Population Based ◽  
Androgen Excess ◽  
Abnormal Glucose Metabolism ◽  
Increased Risk

Abstract Study question What is the role of androgen excess as a contributing factor to insulin resistance and abnormal glucose metabolism (AGM) in women? Summary answer There was a positive association between early adulthood hyperandrogenaemia with AGM. Serum SHBG levels could help identifying women at risk for disordered glucose metabolism. What is known already It is commonly recognised that insulin resistance induces compensatory hyperinsulinaemia which promotes ovarian androgen secretion. Studies in rodents have also suggested that testosterone causes prolonged activation of androgen receptor in pancreatic islet β-cells, inducing insulin hypersecretion and eventually secondary β-cell failure, thus predisposing to type 2 diabetes (T2D). However, the exact physiology behind the association between androgens, insulin resistance and T2D in women is not well understood. Many previously published studies are limited by cross-sectional study design, unrepresentative clinic populations, as well as variying steroid hormone measurement methods and definitions of androgen excess. Study design, size, duration A prospective longitudinal population-based cohort (n = 5,889) to investigate whether serum levels of testosterone (T, measured using LC-MS/MS) and free androgen index (FAI) at ages 31 and 46 associated with AGM at age 46 years. After exclusion of pregnant women, users of hormonal intrauterine device, contraceptive pills, hormone therapy, minipills and statins, there were 4,421 women at age 31 and 4,457 women at age 46. At age 46 a two-hour OGTT was performed in 2,780 women. Participants/materials, setting, methods Serum fasting glucose and insulin, insulin resistance (HOMA–IR) and pancreatic β-cell function (HOMA–B) assessments were performed at ages 31 and 46. Elevated T levels (age 31: >2.3nmol/l; age 46: >1.7nmol/l) were defined according to the 97.5% percentile. T2D diagnoses were gathered from postal questionnaire at age 46, and verified and completed from the hospital discharge and national medication reimbursement registers. Impaired fasting glucose, impaired glucose tolerance or T2D were categorised as AGM. Main results and the role of chance At age 31, hyperandrogenic (HA) women displayed increased insulin resistance estimated by HOMA-IR (1.35±0.96 vs. 1.03±0.44, P = 0.05), increased insulin secretion estimated by HOMA-B (115.05±34.67 vs. 99.25±25.47, P = 0.006), and higher fasting insulin level (10.48±7.54 mU/l vs. 7.93±3.42 mU/l, P = 0.034) compared with normoandrogenic (NA) women, after BMI adjustment. At age 46, HA women had comparable HOMA-B levels (98.04±60.03 vs. 96.27±65.89, P = 0.93) but their fasting glucose (5.57±1.06 mmol/l vs. 5.37±0.77 mmol/, P = 0.07) and glycated haemoglobin levels (37.47±7.83 mmol/mol vs. 36.18±4.99 mmol/mol, P = 0.07) tended to be higher. Women in the highest T quartile (Q4 odds ratio [OR]=1.77, 95%CI: [1.14–2.76]) and in the two highest FAI quartiles at age 31 (Q4: OR = 3.61 [2.16–6.03] and Q3: OR = 2.11 [1.24–3.59]) had increased risk for AGM at age 46, independently of BMI, when compared with women in the lowest quartile. Similarly, women in the two highest FAI quartiles at age 46 had increased risk for AGM (Q4: OR = 2.91 [1.82–4.64]) when compared with women in the lowest quartile, after BMI adjustment. The three highest sex hormone-binding globulin (SHBG) quartiles inversely associated with AGM, both at ages 31 and 46, independently of BMI (at age 31: Q4: OR = 0.38 [0.24–0.62], at age 46: Q4: OR = 0.27 [0.17–0.44]). Limitations, reasons for caution We used only serum T as a marker of HA, even though other androgens, such as androstenedione and adrenal androgens have a place in the evaluation of androgenicity in women. Further studies of other large populations are needed to confirm our results. Wider implications of the findings This is the first longitudinal, general population based study to confirm a positive association between early adulthood hyperandrogenaemia with AGM in middle adulthood independently of confounding factors. Our results further suggest that SHBG levels could help to identify women at risk for AGM. Trial registration number NA

scholarly journals Disturbance in glucose metabolism in patients with lichen planus

2016 ◽  
Vol 9 (4) ◽  
pp. 177
Author(s):  
A. S. M. Zakaria ◽  
Md. Kamal Hossain ◽  
Mohammed Saiful Islam Bhuiyan ◽  
Abida Sultana ◽  
Mahmudur Rahman ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Lichen Planus ◽  
Resistance Index ◽  
Abnormal Glucose Metabolism ◽  
Insulin Resistance Index ◽  
The Mean ◽  
Level 2

<p>The aim of this study was to see the association of lichen planus (n=80) with glucose metabolism disturbance. Classic variety of lichen planus was the most common (76.3%), followed by ashy dermatosis, hypertrophic, oral, actinic and nail lichen planus. The blood glucose level 2 hours after glucose drink was abnormal in 20 cases. HbA<sub>1</sub>c was abnormal in 7 cases. The mean homeostasis model of assessment formulation- insulin resistance index (HOMA-IR) was 2.1 ± 1.6 and it was higher (&gt;4.8) in 12.5% patients. Diabetes mellitus was found in 30 patients. Impaired glucose tolerance was found in 15 cases and high HOMA-IR was found in 10 cases. Total number of cases of abnormal glucose metabolism was found in 55 (68.8%) cases of lichen planus. In conclusion, patients with lichen planus  have higher risk of abnormal glucose metabolism specially diabetes mellitus.</p>

scholarly journals Metformin protects against insulin resistance induced by high uric acid in cardiomyocytes via AMPK signaling pathways in vitro and in vivo

2021 ◽  
Author(s):  
Zhenyu Jiao ◽  
Yingqun Chen ◽  
Yang Xie ◽  
Yanbing Li ◽  
Zhi Li
Keyword(s):  
Insulin Resistance ◽  
Uric Acid ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Abnormal Glucose Metabolism ◽  
Insulin Tolerance

Abstract BackgroundHigh uric acid (HUA) is associated with insulin resistance and abnormal glucose metabolism in cardiomyocytes. Metformin is a recognized agonist of AMP-activated protein kinase (AMPK) and an antidiabetic drug widely used for type 2 diabetes. It can play a cardioprotective role in many pathways. We investigated whether metformin protects against HUA-induced insulin resistance and abnormal glucose metabolism in cardiomyocytes.MethodsWe exposed primary cardiomyocytes to HUA, and cellular glucose uptake was quantified by measuring the uptake of 2-NBDG, a fluorescent glucose analog, after insulin excitation.ResultsTreatment with metformin (10 µmol/L) protected against HUA-inhibited glucose uptake induced by insulin in primary cardiomyocytes, as shown by fluorescence microscopy and flow cytometry analysis. HUA directly inhibited the phosphorylation of Akt and the translocation of glucose transporter type 4 (GLUT4) induced by insulin, which was blocked by metformin. Metformin promoted phosphorylation of AMPK, renewed HUA-inhibited glucose uptake induced by insulin and protected against insulin resistance in cardiomyocytes. As a result of these effects, in a mouse model of acute hyperuricemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. As expected, AICAR, another AMPK activator, had equivalent effects to metformin, demonstrating the important role of AMPK activation in protecting against insulin resistance induced by HUA in cardiomyocytes. Metformin protects against insulin resistance induced by HUA in cardiomyocytes and improves insulin tolerance and glucose tolerance in an acute hyperuricemic mouse model, along with the activation of AMPK.ConclusionsConsequently, metformin may be an important potential new treatment strategy for hyperuricemia-related cardiovascular disease.

scholarly journals Metformin protects against insulin resistance induced by high uric acid in cardiomyocytes via AMPK signaling pathways in vitro and in vivo

2021 ◽  
Author(s):  
Zhenyu Jiao ◽  
Yingqun Chen ◽  
Yang Xie ◽  
Yanbing Li ◽  
Zhi Li
Keyword(s):  
Insulin Resistance ◽  
Uric Acid ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Abnormal Glucose Metabolism ◽  
Insulin Tolerance ◽  
High Uric Acid

AbstractHigh uric acid (HUA) is associated with insulin resistance and abnormal glucose metabolism in cardiomyocytes. Metformin is a recognized agonist of AMP-activated protein kinase (AMPK) and an antidiabetic drug widely used for type 2 diabetes. It can play a cardioprotective role in many pathways. We investigated whether metformin protects against HUA-induced insulin resistance and abnormal glucose metabolism in cardiomyocytes. We exposed primary cardiomyocytes to HUA, and cellular glucose uptake was quantified by measuring the uptake of 2-NBDG, a fluorescent glucose analog, after insulin excitation. Treatment with metformin (10 μmol/L) protected against HUA-inhibited glucose uptake induced by insulin in primary cardiomyocytes, as shown by fluorescence microscopy and flow cytometry analysis. HUA directly inhibited the phosphorylation of Akt and the translocation of glucose transporter type 4 (GLUT4) induced by insulin, which was blocked by metformin. Metformin promoted phosphorylation of AMPK, renewed HUA-inhibited glucose uptake induced by insulin and protected against insulin resistance in cardiomyocytes. As a result of these effects, in a mouse model of acute hyperuricemia, metformin improved insulin tolerance and glucose tolerance, accompanied by increased AMPK phosphorylation, Akt phosphorylation and translocation of GLUT4 in myocardial tissues. As expected, AICAR, another AMPK activator, had equivalent effects to metformin, demonstrating the important role of AMPK activation in protecting against insulin resistance induced by HUA in cardiomyocytes. Metformin protects against insulin resistance induced by HUA in cardiomyocytes and improves insulin tolerance and glucose tolerance in an acute hyperuricemic mouse model, along with the activation of AMPK. Consequently, metformin may be an important potential new treatment strategy for hyperuricemia-related cardiovascular disease.

scholarly journals Hyperandrogenemia in Early Adulthood Is an Independent Risk Factor for Abnormal Glucose Metabolism in Middle Age

2021 ◽  
Author(s):  
Katri Tuorila ◽  
Meri-Maija Ollila ◽  
Marjo-Riitta Järvelin ◽  
Juha S Tapanainen ◽  
Stephen Franks ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Cell Function ◽  
Middle Age ◽  
Early Adulthood ◽  
Serum Testosterone ◽  
Sex Hormone Binding Globulin ◽  
Free Androgen Index ◽  
Abnormal Glucose Metabolism ◽  
Increased Risk

Abstract Context The role of androgen excess as a contributing factor to abnormal glucose metabolism (AGM) and insulin resistance in women remains controversial. Objective To investigate whether hyperandrogenemia (HA) estimated by serum testosterone (T) level and free androgen index (FAI) at ages 31 and 46 is associated with insulin resistance, insulin secretion and AGM by age 46. Design Prospective study including 5,889 females followed at ages 31 and 46. Setting General community. Participants Women with HA were compared with normoandrogenic women at ages 31 and 46. Intervention None. Main outcome measurements AGM, including pre-diabetes and T2DM, homeostatic model assessments of insulin resistance (HOMA–IR) and of pancreatic β-cell function (HOMA–B). Results At age 31, HA women displayed increased HOMA–IR P=0.05), HOMA–B (P=0.006), and higher fasting insulin (P=0.034) than normoandrogenic women after adjusting for body mass index (BMI). At age 46, there was a nonsignificant trend towards higher fasting glucose (P=0.07) and glycated hemoglobin A1 (P=0.067) levels in HA women. Women in the highest T quartile (odds ratio [OR]= 1.80;95%CI, 1.15–2.82) at age 31 and in the two highest FAI quartiles at ages 31 (Q4:OR=3.76;95%CI, 2.24–6.32) and 46 (Q4:OR=2.79;95%CI, 1.74–4.46) had increased risk for AGM, independently of BMI, when compared with women in Q1. Sex hormone-binding globulin (SHBG) was inversely associated with AGM (at age 31:Q4:OR=0.37;95%CI, 0.23–0.60, at age 46:Q4:OR=0.28;95%CI, 0.17–0.44). Conclusion Hyperandrogenemia and low SHBG in early and middle age associates with AGM independently of BMI.

Progression from impaired glucose tolerance to type 2 diabetes in obese children and adolescents: a 3–6-year cohort study in southern Thailand

2016 ◽  
Vol 0 (0) ◽  
Author(s):  
Somchit Jaruratanasirikul ◽  
Sudarat Thammaratchuchai ◽  
Maneerat Puwanant ◽  
Ladda Mo-suwan ◽  
Hutcha Sriplung
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Children And Adolescents ◽  
Weight Status ◽  
Obese Children ◽  
Abnormal Glucose Metabolism

AbstractBackground:Childhood obesity is associated with abnormal glucose metabolism and type 2 diabetes mellitus (T2DM). This study evaluated the prevalence of abnormal glucose metabolism in asymptomatic obese children and adolescents, and determined the percentage of T2DM development after 3–6 years of follow-up.Methods:During 2007–2013, 177 obese children and adolescents who had normal fasting plasma glucose (FPG<100 mg/dL) were given an oral glucose tolerance test (OGTT). The participants were classified into four groups: normal glucose tolerance (NGT), NGT-hyperinsulinemia (NGT-HI), impaired glucose tolerance (IGT), and diabetes mellitus (DM). Blood chemistries, including FPG, glycated hemoglobin, and lipid profiles, and liver function test were performed every 6–12 months or when the patient developed any symptom or sign indicative of diabetes.Results:Glucose metabolism alterations were detected in 81.4% of the participants: 63.8% with NGT-HI, 15.3% with IGT, and 2.3% with T2DM. The median levels of homeostasis model assessment-insulin resistance (HOMA-IR) in patients with IGT (8.63) were significantly greater than those in the patients with NGT (4.04) (p<0.01). During the follow-up, 22 patients (14.4%) developed T2DM significantly more from the IGT group (nine of 33 cases, 27.3%) than the NGT-HI group (12 of 108 cases, 11.1%) (p=0.022). The predicting parameters for T2DM conversion were weight status, body mass index (BMI), FBG, fasting insulin, alanine transaminase (ALT) levels, and HOMA-IR.Conclusions:Glucose metabolism alteration was commonly found among obese adolescents. Factors associated with T2DM development were greater weight status and the severity of insulin resistance as shown by higher HOMA-IR levels.

scholarly journals Relationship of Serum Fibroblast Growth Factor 21 with Abnormal Glucose Metabolism and Insulin Resistance: The Baltimore Longitudinal Study of Aging

2012 ◽  
Vol 97 (4) ◽  
pp. 1375-1382 ◽  
Author(s):  
Richard D. Semba ◽  
Kai Sun ◽  
Josephine M. Egan ◽  
Candace Crasto ◽  
Olga D. Carlson ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Community Dwelling ◽  
Fibroblast Growth Factor 21 ◽  
Abnormal Glucose Metabolism ◽  
Matsuda Index ◽  
Baltimore Longitudinal Study ◽  
Relationship Of ◽  
The Relationship

Context: The relationship of fibroblast growth factor 21 (FGF21) with glucose metabolism and insulin resistance has not been well characterized in community-dwelling adults. Objective: The objective of the study was to examine the relationship of FGF21 with glucose metabolism and insulin resistance. Design: Serum FGF21, fasting plasma glucose (FPG), glucose tolerance, and insulin resistance were measured in a cross-sectional study, 2002–2007. Setting: The study was the Baltimore Longitudinal Study of Aging, a natural history cohort study of aging in community-dwelling men and women. Participants: Seven hundred adults, mean age 63.3 yr, participated in the study. Main Outcome Measures: FPG, 2-h plasma glucose, homeostasis model of insulin resistance, whole-body insulin sensitivity (Matsuda index), glucose area under the curve (AUC), and insulin AUC were measured. Results: Overall, the median (25th and 75th percentiles) FGF21 concentration was 225 (126, 370) pg/ml. The proportion of adults with normal, impaired, and diabetic FPG was 77.0, 21.4, and 1.6%, and those with normal, impaired, and diabetic 2-h plasma glucose was 76.7, 19.1, and 4.1%, respectively. Log serum FGF21 (picograms per milliliter), per 1 sd increase, was associated with an FPG (odds ratio 1.43, 95% confidence interval 1.15, 1.77, P = 0.001) and with 2-h plasma glucose (odds ratio 1.39, 95% confidence interval 1.12, 1.73, P = 0.003), in respective multivariate, ordered logistic regression models, adjusted for potential confounders. Serum FGF21 (picograms per milliliter) was associated with the homeostasis model of insulin resistance, the Matsuda index, glucose AUC, and insulin AUC (all P &lt; 0.0001) in respective multivariable linear regression models adjusted for potential confounders. Conclusions: Higher serum FGF21 concentrations were associated with abnormal glucose metabolism and insulin resistance in community-dwelling adults.

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