The Effect of Glucose on Glucagon-Like Peptide-1 Secretion in Hispanic Adults With Type Two Diabetes Mellitus, Impaired Glucose Tolerance, or Normal Glucose Tolerance

2016 ◽  
Vol 116 (9) ◽  
pp. A95
Author(s):  
E. Adams ◽  
P. Genter ◽  
V. Gray ◽  
E. Ipp
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Hispanic Adults ◽  
Normal Glucose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Type Two Diabetes ◽  
Effect Of Glucose

“A COMPARATIVE STUDY OF NERVE CONDUCTION VELOCITIES IN INDIVIDUALS WITH NORMALAND IMPAIRED GLUCOSE TOLERANCE”

2021 ◽  
pp. 49-51
Author(s):  
B.V.K. Vijayalakshmi ◽  
P.Nanda Kumar ◽  
Shaik Auliya Parveen
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Conduction Velocity ◽  
Nerve Conduction ◽  
Nerve Conduction Velocity ◽  
Normal Glucose Tolerance ◽  
Abnormal Glucose Metabolism ◽  
Normal Glucose ◽  
Prevalence Of Diabetes Mellitus

INTRODUCTION: Diabetes mellitus is a global problem. The prevalence of diabetes mellitus is growing rapidly worldwide and is reaching epidemic proportions. Diabetic neuropathy is the most common and troublesome complication of diabetes mellitus, accounting for 28%, leading to great morbidity and resulting in a huge economic burden for diabetes care. AIMS AND OBJECTIVES: AIM To look for changes in Nerve Conduction Velocity in early stages of Glucose Intolerance i.e. in Impaired Glucose Tolerance (IGT). OBJECTIVES: To determine the Nerve Conduction Velocity of Peripheral Nerve in lower limb in Normal Glucose Tolerance (NGT) subjects, IGT patients. To compare and analyze Motor NCV of Peroneal Nerve and Sensory NCV of Sural Nerve in Normal Glucose Tolerance subjects, IGTpatients. MATERIALS AND METHODS: 50 subjects with normal glucose tolerance and 50 subjects with impaired glucose tolerance were selected and the study was conducted in Government General Hospital, Guntur. RESULTS AND OBSERVATIONS:there are signicant changes in latency, amplitude and velocity in the 2 groups. CONCLUSION: The early detection of abnormal glucose metabolism is particularly important, as treatments will probably be most effective if administered early in the course of neuropathy,

scholarly journals Significance of Pro12Ala Mutation in Peroxisome Proliferator-Activated Receptor-γ2 in Korean Diabetic and Obese Subjects*

2000 ◽  
Vol 85 (5) ◽  
pp. 1801-1804 ◽  
Author(s):  
Eun Young Oh ◽  
Kyeong Min Min ◽  
Jae Hoon Chung ◽  
Yong-Ki Min ◽  
Myung-Shik Lee ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Nuclear Hormone Receptor ◽  
Allele Frequencies ◽  
Peroxisome Proliferator ◽  
Normal Glucose ◽  
Obese Subjects ◽  
The Relationship

Abstract Peroxisome proliferator-activated receptors (PPARs) are a nuclear hormone receptor superfamily of ligand-activated transcription factors, and the PPARγ subtype regulates adipocyte differentiation, lipid metabolism, and insulin sensitivity. There have been several reports on the relationship between the PPARγ2 Pro12Ala genotype and obesity or diabetes in Caucasians. The objective of this study was to examine the relationship between this mutation and obesity or diabetes in Korean subjects. Two hundred and twenty-nine Korean subjects, including 111 obese subjects (body mass index, >25 kg/m2) were included in this study. One hundred and eleven subjects had normal glucose tolerance, 60 had impaired glucose tolerance, and 58 had diabetes mellitus. We evaluated these subjects for the Pro12Ala mutation in the PPARγ gene using PCR-restriction fragment length polymorphism. Allele frequencies of the Pro12Ala missense mutation of PPARγ2 were not different among Korean subjects with normal glucose tolerance (qAla = 0.045), those with impaired glucose tolerance (qAla = 0.033), and those with diabetes mellitus (qAla = 0.043; P> 0.05). Allele frequencies of PPARγ2 Ala in obese subjects (qAla = 0.036) were not significantly different from those in nonobese subjects (qAla = 0.047). These results suggest that the Pro12Ala mutation in PPARγ is not associated with either diabetes or obesity and may not be an important determinant of obesity or diabetes in Korean subjects.

Impact of Glucose Metabolism Disorders on IGF-1 Levels in Patients with Acromegaly

2018 ◽  
Vol 50 (05) ◽  
pp. 408-413 ◽  
Author(s):  
Sema Dogansen ◽  
Gulsah Yalin ◽  
Seher Tanrikulu ◽  
Sema Yarman
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Glucose Metabolism Disorders ◽  
Insulin Resistant ◽  
Normal Glucose ◽  
Resistant Group ◽  
The Impact

AbstractIn this study, we aimed to evaluate the presence of glucose metabolism abnormalities and their impact on IGF-1 levels in patients with acromegaly. Ninety-three patients with acromegaly (n=93; 52 males/41 females) were included in this study. Patients were separated into three groups such as; normal glucose tolerance (n=23, 25%), prediabetes (n=38, 41%), and diabetes mellitus (n=32, 34%). Insulin resistance was calculated with homeostasis model assessment (HOMA). HOMA-IR > 2.5 or ≤2.5 were defined as insulin resistant or noninsulin resistant groups, respectively. Groups were compared in terms of factors that may be associated with glucose metabolism abnormalities. IGF-1% ULN (upper limit of normal)/GH ratios were used to evaluate the impact of glucose metabolism abnormalities on IGF-1 levels. Patients with diabetes mellitus were significantly older with an increased frequency of hypertension (p<0.001, p=0.01, respectively). IGF-1% ULN/GH ratio was significantly lower in prediabetes group than in normal glucose tolerance group (p=0.04). Similarly IGF-1% ULN/GH ratio was significantly lower in insulin resistant group than in noninsulin resistant group (p=0.04). Baseline and suppressed GH levels were significantly higher in insulin resistant group than in noninsulin resistant group (p=0.024, p<0.001, respectively). IGF-1% ULN/GH ratio is a useful marker indicating glucose metabolism disorders and IGF-1 levels might be inappropriately lower in acromegalic patients with insulin resistance or prediabetes. We suggest that IGF-1 levels should be re-evaluated after the improvement of insulin resistance or glycemic regulation for the successful management of patients with acromegaly.

Progression of normal glucose tolerance to impaired glucose tolerance or diabetes in the elderly

1997 ◽  
Vol 35 (2-3) ◽  
pp. 99-106 ◽  
Author(s):  
Liisa Hiltunen ◽  
Sirkka-Liisa Kivelä ◽  
Esa Läärä ◽  
Sirkka Keinänen-Kiukaanniemi
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
The Elderly ◽  
Normal Glucose Tolerance ◽  
Normal Glucose

scholarly journals Pax6 Haploinsufficiency Causes Abnormal Metabolic Homeostasis by Down-Regulating Glucagon-Like Peptide 1 in Mice

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2136-2144 ◽  
Author(s):  
Jun Ding ◽  
Yan Gao ◽  
Jing Zhao ◽  
Hong Yan ◽  
Shi-ying Guo ◽  
...  
Keyword(s):  
Food Intake ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Mutant Mouse ◽  
Metabolic Abnormalities ◽  
Metabolic Homeostasis ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
In Vitro Transfection

Heterozygosity for the Pax6 allele is associated with impaired glucose tolerance in humans. With a Pax6 mutant mouse model, we found many of the metabolic abnormalities were consistent with the effects of down-regulating the expression of glucagon-like peptide 1 (GLP-1). In addition to impaired glucose tolerance, adult heterozygous mutant mice (Pax6m/+) secreted less insulin responding to glucose and arginine administration compared with control mice. Moreover, Pax6m/+ mice showed increased food intake compared with control mice, although they were resistant to diet-induced fat accumulation. Indeed, levels of circulating GLP-1 and intestinal transcription of Gcg/Proglucagon were dramatically reduced in Pax6m/+ mice. Mutated Pax6 also failed to activate the Gcg/Proglucagon promoter by in vitro transfection assay. Finally, administering the GLP-1 receptor agonist exendin-4 to Pax6m/+ mice largely reversed their abnormal food intake, glycemic excursion, and insulin secretion. Our studies suggested that disruption of metabolic homeostasis mainly caused by Pax6 haploinsufficiency was mainly mediated by down-regulation of GLP-1. Administration of exendin-4 may be a useful therapy in humans with a similar mutation.

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