scholarly journals Pathophysiology and Pharmacological Treatment of Insulin Resistance*

2000 ◽  
Vol 21 (6) ◽  
pp. 585-618 ◽  
Author(s):  
Stephan Matthaei ◽  
Michael Stumvoll ◽  
Monika Kellerer ◽  
Hans-Ulrich Häring
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Progressive Disease ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Pharmacological Agents ◽  
Cell Dysfunction ◽  
Glucosidase Inhibitors ◽  
Type 2 Diabetic

Abstract Diabetes mellitus type 2 is a world-wide growing health problem affecting more than 150 million people at the beginning of the new millennium. It is believed that this number will double in the next 25 yr. The pathophysiological hallmarks of type 2 diabetes mellitus consist of insulin resistance, pancreatic β-cell dysfunction, and increased endogenous glucose production. To reduce the marked increase of cardiovascular mortality of type 2 diabetic subjects, optimal treatment aims at normalization of body weight, glycemia, blood pressure, and lipidemia. This review focuses on the pathophysiology and molecular pathogenesis of insulin resistance and on the capability of antihyperglycemic pharmacological agents to treat insulin resistance, i.e., α-glucosidase inhibitors, biguanides, thiazolidinediones, sulfonylureas, and insulin. Finally, a rational treatment approach is proposed based on the dynamic pathophysiological abnormalities of this highly heterogeneous and progressive disease.

scholarly journals Insulin Resistance and Diabetes Mellitus in Alzheimer’s Disease

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1236
Author(s):  
Jesús Burillo ◽  
Patricia Marqués ◽  
Beatriz Jiménez ◽  
Carlos González-Blanco ◽  
Manuel Benito ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Alzheimer's Disease ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Progressive Disease

Type 2 diabetes mellitus is a progressive disease that is characterized by the appearance of insulin resistance. The term insulin resistance is very wide and could affect different proteins involved in insulin signaling, as well as other mechanisms. In this review, we have analyzed the main molecular mechanisms that could be involved in the connection between type 2 diabetes and neurodegeneration, in general, and more specifically with the appearance of Alzheimer’s disease. We have studied, in more detail, the different processes involved, such as inflammation, endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction.

scholarly journals Spontaneous Type 2 Diabetic Rodent Models

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yang-wei Wang ◽  
Guang-dong Sun ◽  
Jing Sun ◽  
Shu-jun Liu ◽  
Ji Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Health Care ◽  
Animal Models ◽  
Rodent Models ◽  
Advantages And Disadvantages ◽  
Characteristic Features ◽  
Type 2 Diabetic

Diabetes mellitus, especially type 2 diabetes (T2DM), is one of the most common chronic diseases and continues to increase in numbers with large proportion of health care budget being used. Many animal models have been established in order to investigate the mechanisms and pathophysiologic progress of T2DM and find effective treatments for its complications. On the basis of their strains, features, advantages, and disadvantages, various types of animal models of T2DM can be divided into spontaneously diabetic models, artificially induced diabetic models, and transgenic/knockout diabetic models. Among these models, the spontaneous rodent models are used more frequently because many of them can closely describe the characteristic features of T2DM, especially obesity and insulin resistance. In this paper, we aim to investigate the current available spontaneous rodent models for T2DM with regard to their characteristic features, advantages, and disadvantages, and especially to describe appropriate selection and usefulness of different spontaneous rodent models in testing of various new antidiabetic drugs for the treatment of type 2 diabetes.

Effect of IGF-I on FFA and glucose metabolism in control and type 2 diabetic subjects

2002 ◽  
Vol 282 (6) ◽  
pp. E1360-E1368 ◽  
Author(s):  
Thongchai Pratipanawatr ◽  
Wilailak Pratipanawatr ◽  
Clifford Rosen ◽  
Rachele Berria ◽  
Mandeep Bajaj ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Glucose Disposal ◽  
Insulin Resistant ◽  
Control Subjects ◽  
Igf I ◽  
Plasma Ffa ◽  
Type 2 Diabetic

The effects of insulin-like growth factor I (IGF-I) and insulin on free fatty acid (FFA) and glucose metabolism were compared in eight control and eight type 2 diabetic subjects, who received a two-step euglycemic hyperinsulinemic (0.25 and 0.5 mU · kg−1 · min−1) clamp and a two-step euglycemic IGF-I (26 and 52 pmol · kg−1 · min−1) clamp with [3-3H]glucose, [1-14C]palmitate, and indirect calorimetry. The insulin and IGF-I infusion rates were chosen to augment glucose disposal (Rd) to a similar extent in control subjects. In type 2 diabetic subjects, stimulation of Rd (second clamp step) in response to both insulin and IGF-I was reduced by ∼40–50% compared with control subjects. In control subjects, insulin was more effective than IGF-I in suppressing endogenous glucose production (EGP) during both clamp steps. In type 2 diabetic subjects, insulin-mediated suppression of EGP was impaired, whereas EGP suppression by IGF-I was similar to that of controls. In both control and diabetic subjects, IGF-I-mediated suppression of plasma FFA concentration and inhibition of FFA turnover were markedly impaired compared with insulin ( P < 0.01–0.001). During the second IGF-I clamp step, suppression of plasma FFA concentration and FFA turnover was impaired in diabetic vs. control subjects ( P < 0.05–0.01). Conclusions: 1) IGF-I is less effective than insulin in suppressing EGP and FFA turnover; 2) insulin-resistant type 2 diabetic subjects also exhibit IGF-I resistance in skeletal muscle. However, suppression of EGP by IGF-I is not impaired in diabetic individuals, indicating normal hepatic sensitivity to IGF-I.

scholarly journals Risk Factors for Type 2 Diabetes Mellitus Preceded by β-Cell Dysfunction, Insulin Resistance, or Both in Older Adults

2013 ◽  
Vol 177 (12) ◽  
pp. 1418-1429 ◽  
Author(s):  
Fumiaki Imamura ◽  
Kenneth J. Mukamal ◽  
James B. Meigs ◽  
José A. Luchsinger ◽  
Joachim H. Ix ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Older Adults ◽  
Type 2 Diabetes Mellitus ◽  
Β Cell ◽  
Cell Dysfunction

Potential Effects of Nonsteroidal Anti-Inflammatory Drugs in the Prevention and Treatment of Type 2 Diabetes Mellitus

2016 ◽  
Vol 30 (5) ◽  
pp. 549-556 ◽  
Author(s):  
Pamela Natalia Bellucci ◽  
María Florencia González Bagnes ◽  
Guillermo Di Girolamo ◽  
Claudio Daniel González
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Metabolic Effects ◽  
Analgesic Effects ◽  
Peripheral Insulin Resistance ◽  
Patients With Diabetes ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of heterogeneous drugs largely known for their anti-inflammatory, antipyretic, and analgesic effects, which are met by means of the inhibition of the cyclooxygenase (COX) enzymes. Even when their use in patients with diabetes mellitus is limited due to relevant adverse events, some pharmacological and metabolic effects of NSAIDs have been further studied to be potentially beneficial in the prevention and/or treatment of diabetic subjects. Effects on endogenous glucose production, peripheral insulin resistance, pancreatic islet, and systemic inflammation and the insulin clearance have been reported. In this article, we overview the scientific literature of the last 5 years regarding the potential effects of NSAID treatment on diabetes prevention/treatment. The selected papers showed information in both humans and animal models. Furthermore, we included papers that suggest new areas for further investigation, and we discussed our own suggestions on this matter.

scholarly journals Possibilities of application a fixed combination of alogliptin and pioglitazone for type 2 diabetes mellitus treatment

2021 ◽  
Vol 24 (2) ◽  
pp. 193-197
Author(s):  
M. V. Shestakova ◽  
M. B. Antsiferov ◽  
A. S. Ametov ◽  
G. R. Galstyan ◽  
T. Y. Demidova ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Fixed Combination ◽  
Glucose Production ◽  
Clinical Problem ◽  
Cell Dysfunction ◽  
Steady Decrease ◽  
Diabetes Mellitus Treatment ◽  
Excess Glucose

Hyperglycemia in T2DM is based on three main mechanisms: insulin resistance, progressive β-cell dysfunction, and excess glucose production by the liver.The onset of T2DM is usually preceded by a long period of insulin resistance. Prescribing sugar drugs that affect different links of pathogenesis, reducing a steady decrease in glycemia. To date, in clinical practice, various combinations of hypoglycemic drugs are used, the choice of which is determined by the characteristics of the course of diabetes in the patient, the presence of concomitant diseases and complications of diabetes, as well as the dominant clinical problem. This resolution provides an expert council opinion on the feasibility of using a combination of alogliptin and pioglitazone in patients with type 2 diabetes.

scholarly journals Assessment of vitamin D status and its association with insulin resistance among type 2 diabetic subjects

2018 ◽  
Vol 6 (12) ◽  
pp. 3825
Author(s):  
Jaitra Bhattacharya
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Serum Vitamin ◽  
Serum Vitamin D ◽  
Vitamin D Levels ◽  
Type 2 Diabetic

Background: The 21st century has seen the rise of diabetes mellitus as one of the major metabolic issues as is vitamin D deficiency which has been found to be pandemic worldwide. The present study is an endeavor to study the status of serum vitamin D levels in relation to the glycemic and insulin resistance status in type 2 diabetes mellitus patients.Methods: The present is a cross-sectional study with a sample size of 100 type 2 diabetic subjects in the age group of 30-60 years. Serum vitamin D and Insulin levels were estimated using the ELISA technique. HbA1c levels were measured using immunoturbidimetric assays and plasma glucose levels were determined using glucose oxidase- peroxidase method.Results: The fasting plasma glucose, HbA1c and serum insulin levels were found to be significantly higher in those with vitamin D levels below the normal cut-off value of less than 30ng/ml (p value <0.01). Also, the insulin resistance calculated using HOMA-IR was found to be higher in those subjects having vitamin D deficiency or insufficiency.Conclusions: Hence, the study suggests that vitamin D deficiency contributes to further insulin resistance and poorer long-term diabetic control in type 2 diabetes mellitus subjects.

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