Association of mitochondrial dysfunction and lipid metabolism with type 2 diabetes mellitus: A review of literature

2018 ◽  
Vol 13 (6) ◽  
pp. 406-417
Author(s):  
Karimeh Haghani ◽  
Pouyan Asadi ◽  
Gholamreza Taheripak ◽  
Ali Noori-Zadeh ◽  
Shahram Darabi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Mitochondrial Dysfunction ◽  
Review Of Literature

scholarly journals Transcriptional Profiling and Biological Pathway(s) Analysis of Type 2 Diabetes Mellitus in a Pakistani Population

2020 ◽  
Vol 17 (16) ◽  
pp. 5866
Author(s):  
Zarish Noreen ◽  
Christopher A. Loffredo ◽  
Attya Bhatti ◽  
Jyothirmai J. Simhadri ◽  
Gail Nunlee-Bland ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Health Concern ◽  
Receptor Signaling ◽  
Small Pilot Study

The epidemic of type 2 diabetes mellitus (T2DM) is an important global health concern. Our earlier epidemiological investigation in Pakistan prompted us to conduct a molecular investigation to decipher the differential genetic pathways of this health condition in relation to non-diabetic controls. Our microarray studies of global gene expression were conducted on the Affymetrix platform using Human Genome U133 Plus 2.0 Array along with Ingenuity Pathway Analysis (IPA) to associate the affected genes with their canonical pathways. High-throughput qRT-PCR TaqMan Low Density Array (TLDA) was performed to validate the selected differentially expressed genes of our interest, viz., ARNT, LEPR, MYC, RRAD, CYP2D6, TP53, APOC1, APOC2, CYP1B1, SLC2A13, and SLC33A1 using a small population validation sample (n = 15 cases and their corresponding matched controls). Overall, our small pilot study revealed a discrete gene expression profile in cases compared to controls. The disease pathways included: Insulin Receptor Signaling, Type II Diabetes Mellitus Signaling, Apoptosis Signaling, Aryl Hydrocarbon Receptor Signaling, p53 Signaling, Mitochondrial Dysfunction, Chronic Myeloid Leukemia Signaling, Parkinson’s Signaling, Molecular Mechanism of Cancer, and Cell Cycle G1/S Checkpoint Regulation, GABA Receptor Signaling, Neuroinflammation Signaling Pathway, Dopamine Receptor Signaling, Sirtuin Signaling Pathway, Oxidative Phosphorylation, LXR/RXR Activation, and Mitochondrial Dysfunction, strongly consistent with the evidence from epidemiological studies. These gene fingerprints could lead to the development of biomarkers for the identification of subgroups at high risk for future disease well ahead of time, before the actual disease becomes visible.

scholarly journals Muscular mitochondrial dysfunction and type 2 diabetes mellitus

2007 ◽  
Vol 10 (6) ◽  
pp. 698-703 ◽  
Author(s):  
Vera B Schrauwen-Hinderling ◽  
Michael Roden ◽  
M Eline Kooi ◽  
Matthijs KC Hesselink ◽  
Patrick Schrauwen
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Dysfunction

SEX DIFFERENCES OF CARBOHYDRATE AND LIPID METABOLISM IMPAIRMENT IN RATS WITH TYPE 2 DIABETES MELLITUS

2018 ◽  
Vol 64 (2) ◽  
pp. 39-45 ◽  
Author(s):  
Nataliia Gorbenko ◽  
Oleksii Borikov ◽  
Olha Ivanova ◽  
K. V. Taran ◽  
T. S. Litvinova ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Female Rats ◽  
Glucose And Lipid Metabolism ◽  
Carbohydrate And Lipid Metabolism ◽  
Lipid Metabolism Disorders

A sex difference of carbohydrate and lipid metabolism disorders in rats with type 2 diabetes has been studied. It was established that type 2 diabetes leads to a more pronounced deterioration in carbohydrate toleranceand insulin sensitivity in males compared to female rats, but the sex doesn’t affect basal glycemia and fructosamine levels. It was found that the increase of body weight and visceral fat in rats with type 2 diabetes is moremanifested in females than in males. It has been determined that hypertriglyceridemia is higher in diabeticmales compared to diabetic females, and the level of common lipids in the liver, both intact females and femaleswith type 2 diabetes, is lower than that of the males. The obtained results indicate a more expressive impairment of glucose and lipid metabolism in males compared to females with type 2 diabetes

A Systematic Review Exploring Acculturation and Type 2 Diabetes in Spanish-Speaking Populations

2021 ◽  
pp. 154041532110370
Author(s):  
Alyssia M. Miller De Rutté ◽  
Amanda Barrie
Keyword(s):  
Diabetes Mellitus ◽  
United States ◽  
Systematic Review ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
The United States ◽  
Review Of Literature ◽  
Spanish Speaking ◽  
The Relationship

Background: Acculturation to the United States has been previously studied in Spanish-speaking populations, but little is known about the potential relationship between acculturation and type 2 diabetes mellitus (T2DM). Objective: The purpose of this systematic review was to explore the relationship between acculturation and T2DM in Spanish-speaking populations in the United States. Methods: Selected studies collected from a review of literature were analyzed by population, ethnicity, acculturation scale, and significance. Results: Thirty-two eligible articles showed conflicting data between the effects of acculturation on T2DM. Conclusion: Overall, studies yielded inconclusive results on the significance of the relationship between acculturation and diabetes in Spanish-speaking populations, which merit further investigation.

scholarly journals Proanthocyanidins Ameliorated Deficits of Lipid Metabolism in Type 2 Diabetes Mellitus Via Inhibiting Adipogenesis and Improving Mitochondrial Function

2020 ◽  
Vol 21 (6) ◽  
pp. 2029
Author(s):  
Fangfang Tie ◽  
Jifei Wang ◽  
Yuexin Liang ◽  
Shujun Zhu ◽  
Zhenhua Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Mitochondrial Function ◽  
Underlying Mechanism ◽  
Mitochondrial Dysfunctions ◽  
Mitochondrial Mass

Proanthocyanidins are the major active compounds extracted from Iris lactea Pall. var. Chinensis (Fisch.) Koidz (I. lactea). Proanthocyanidins exhibit a variety of pharmacological activities such as anti-oxidation, anti-inflammation, anti-tumor, and lowering blood lipids. However, the underlying mechanism of its regulating effect on lipid metabolism in diabetic conditions remains unclear. The present study investigated the effects of I. lactea-derived proanthocyanidins on lipid metabolism in mice of type 2 diabetes mellitus (T2DM). Results demonstrated a beneficial effect of total proanthocyanidins on dysregulated lipid metabolism and hepatic steatosis in high-fat-diet/streptozocin (STZ)-induced T2DM. To identify the mechanisms, six flavan-3-ols were isolated from proanthocyanidins of I. lacteal and their effects on adipogenesis and dexamethasone (Dex)-induced mitochondrial dysfunctions in 3T3-L1 adipocytes were determined. In vitro studies showed flavan-3-ols inhibited adipogenesis and restored mitochondrial function after Dex-induced insulin resistance, being suggested by increased mitochondrial membrane potential, intracellular ATP contents, mitochondrial mass and mitochondrial biogenesis, and reduced reactive oxygen species. Among the six flavan-3-ols, procyanidin B3 and procyanidin B1 exhibited the strongest effects. Our study suggests potential of proanthocyanidins as therapeutic target for diabetes.

scholarly journals Mitochondrial Dysfunction andβ-Cell Failure in Type 2 Diabetes Mellitus

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Zhongmin Alex Ma ◽  
Zhengshan Zhao ◽  
John Turk
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Dysfunction ◽  
Membrane Integrity ◽  
Metabolic Stress ◽  
Atp Synthesis ◽  
Peripheral Insulin Resistance ◽  
Glucose Stimulated Insulin Secretion

Type 2 diabetes mellitus (T2DM) is the most common human endocrine disease and is characterized by peripheral insulin resistance and pancreatic isletβ-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor toβ-cell failure in the evolution of T2DM. As reviewed elsewhere, reactive oxygen species (ROS) produced byβ-cell mitochondria as a result of metabolic stress activate several stress-response pathways. This paper focuses on mechanisms whereby ROS affect mitochondrial structure and function and lead toβ-cell failure. ROS activate UCP2, which results in proton leak across the mitochondrial inner membrane, and this leads to reducedβ-cell ATP synthesis and content, which is a critical parameter in regulating glucose-stimulated insulin secretion. In addition, ROS oxidize polyunsaturated fatty acids in mitochondrial cardiolipin and other phospholipids, and this impairs membrane integrity and leads to cytochromecrelease into cytosol and apoptosis. Group VIA phospholipase A2(iPLA2β) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA2β-deficiency increasesβ-cell mitochondrial susceptibility to injury from ROS and predisposes to developing T2DM. Interventions that attenuate ROS effects onβ-cell mitochondrial phospholipids might prevent or retard development of T2DM.

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