scholarly journals Exercise Training-Induced Changes in MicroRNAs: Beneficial Regulatory Effects in Hypertension, Type 2 Diabetes, and Obesity

2018 ◽  
Vol 19 (11) ◽  
pp. 3608 ◽  
Author(s):  
Alex Improta Caria ◽  
Carolina Nonaka ◽  
Ciro Pereira ◽  
Milena Soares ◽  
Simone Macambira ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Exercise Training ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Phenotypic Change ◽  
Glucose Levels ◽  
Physiological Processes ◽  
Regulatory Effects

MicroRNAs are small non-coding RNAs that regulate gene expression post-transcriptionally. They are involved in the regulation of physiological processes, such as adaptation to physical exercise, and also in disease settings, such as systemic arterial hypertension (SAH), type 2 diabetes mellitus (T2D), and obesity. In SAH, microRNAs play a significant role in the regulation of key signaling pathways that lead to the hyperactivation of the renin-angiotensin-aldosterone system, endothelial dysfunction, inflammation, proliferation, and phenotypic change in smooth muscle cells, and the hyperactivation of the sympathetic nervous system. MicroRNAs are also involved in the regulation of insulin signaling and blood glucose levels in T2D, and participate in lipid metabolism, adipogenesis, and adipocyte differentiation in obesity, with specific microRNA signatures involved in the pathogenesis of each disease. Many studies report the benefits promoted by exercise training in cardiovascular diseases by reducing blood pressure, glucose levels, and improving insulin signaling and lipid metabolism. The molecular mechanisms involved, however, remain poorly understood, especially regarding the participation of microRNAs in these processes. This review aimed to highlight microRNAs already known to be associated with SAH, T2D, and obesity, as well as their possible regulation by exercise training.

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 Endurance exercise training programs intestinal lipid metabolism in a rat model of obesity and type 2 diabetes

2015 ◽  
Vol 3 (1) ◽  
pp. e12232 ◽  
Author(s):  
Yu-Han Hung ◽  
Melissa A. Linden ◽  
Alicia Gordon ◽  
R. Scott Rector ◽  
Kimberly K. Buhman
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Rat Model ◽  
Training Programs ◽  
Endurance Exercise Training

Estimation of ellagic acid and/or repaglinide effects on insulin signaling, oxidative stress, and inflammatory mediators of liver, pancreas, adipose tissue, and brain in insulin resistant/type 2 diabetic rats

2017 ◽  
Vol 42 (2) ◽  
pp. 181-192 ◽  
Author(s):  
Mohamed M. Amin ◽  
Mahmoud S. Arbid
Keyword(s):  
Type 2 Diabetes ◽  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Signaling ◽  
Inflammatory Mediators ◽  
Ellagic Acid ◽  
Molecular Mechanisms ◽  
Combined Treatment ◽  
Albino Rats

Even though ellagic acid has previously been valued in many models of cancer, so far its full mechanistic effect as a natural antiapoptotic agent in the prevention of type 2 diabetes complications has not been completely elucidated, which was the goal of this study. We fed albino rats a high-fat fructose diet (HFFD) for 2 months to induce insulin resistance/type 2 diabetes and then treated the rats with ellagic acid (10 mg/kg body weight, orally) and/or repaglinide (0.5 mg/kg body weight, orally) for 2 weeks. At the serum level, ellagic acid challenged the consequences of HFFD, significantly improving the glucose/insulin balance, liver enzymes, lipid profile, inflammatory cytokines, redox level, adipokines, ammonia, and manganese. At the tissue level (liver, pancreas, adipose tissue, and brain), ellagic acid significantly enhanced insulin signaling, autophosphorylation, adiponectin receptors, glucose transporters, inflammatory mediators, and apoptotic markers. Remarkably, combined treatment with both ellagic acid and repaglinide had a more pronounced effect than treatment with either alone. These outcomes give new insight into the promising molecular mechanisms by which ellagic acid modulates numerous factors induced in the progression of diabetes.

scholarly journals Exercise training to reduce cardiovascular risk in patients with metabolic syndrome and type 2 diabetes mellitus: How does it work?

2018 ◽  
Vol 26 (7) ◽  
pp. 701-708 ◽  
Author(s):  
Nicolle Kränkel ◽  
Martin Bahls ◽  
Emeline M. Van Craenenbroeck ◽  
Volker Adams ◽  
Luis Serratosa ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Type 2 Diabetes Mellitus ◽  
Cardiovascular Risk ◽  
Exercise Training ◽  
Molecular Mechanisms ◽  
Patient Specific ◽  
Individual Risk

Metabolic syndrome (MetS) – a clustering of pathological conditions, including abdominal obesity, hypertension, dyslipidemia and hyperglycaemia – is closely associated with the development of type 2 diabetes mellitus (T2DM) and a high risk of cardiovascular disease. A combination of multigenetic predisposition and lifestyle choices accounts for the varying inter-individual risk to develop MetS and T2DM, as well as for the individual amount of the increase in cardiovascular risk in those patients. A physically active lifestyle can offset about half of the genetically mediated cardiovascular risk. Yet, the extent to which standardized exercise programmes can reduce cardiovascular risk differs between patients. Exercise parameters, such as frequency, intensity, type and duration or number of repetitions, differentially target metabolic function, vascular health and physical fitness. In addition, exercise-induced molecular mechanisms are modulated by other patient-specific variables, such as age, diet and medication. This review discusses the molecular and cellular mechanisms underlying the effects of exercise training on cardiovascular risk specifically in patients with MetS and T2DM.

scholarly journals Effects of Moderate- Versus High-Intensity Exercise Training on Physical Fitness and Physical Function in People With Type 2 Diabetes: A Randomized Clinical Trial

2014 ◽  
Vol 94 (12) ◽  
pp. 1720-1730 ◽  
Author(s):  
J. David Taylor ◽  
James P. Fletcher ◽  
Ruth Ann Mathis ◽  
W. Todd Cade
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Training ◽  
Physical Fitness ◽  
Physical Function ◽  
High Intensity ◽  
High Intensity Exercise ◽  
High Group ◽  
Glucose Levels ◽  
Intensity Training

Background Exercise training is effective for improving physical fitness and physical function in people with type 2 diabetes. However, limited research has been conducted on the optimal exercise training intensity for this population. Objective The primary study objective was to investigate the effects of moderate- versus high-intensity exercise training on physical fitness and physical function in people with type 2 diabetes. Design This was a randomized clinical trial. Setting The setting was a university campus. Participants Twenty-one people with type 2 diabetes were randomly allocated to receive either moderate-intensity training (MOD group) or high-intensity training (HIGH group). Intervention The MOD group performed resistance training at an intensity of 75% of the 8-repetition maximum (8-RM) and aerobic training at an intensity of 30% to 45% of the heart rate reserve (HRR). The HIGH group performed resistance training at an intensity of 100% of the 8-RM and aerobic training at an intensity of 50% to 65% of the HRR. Measurements Muscle strength (peak torque [newton-meters]), exercise capacity (graded exercise test duration [minutes]), and physical function (Patient-Specific Functional Scale questionnaire) were measured at baseline and 3 months later. Acute exercise-induced changes in glucose levels were assessed immediately before exercise, immediately after exercise, and 1 hour after exercise during the first exercise training session. Results Although both groups showed improvements in physical fitness and physical function, the between-group effect sizes were not statistically significant (exercise capacity estimated marginal mean [EMM] difference=2.1, 95% confidence interval [95% CI]=−0.2, 4.5; muscle strength EMM difference=20.8, 95% CI=−23.3, 65.0; and physical function EMM difference=0.1, 95% CI=−0.6, 0.9). Mean percent changes in glucose levels measured immediately before exercise and immediately after exercise, immediately after exercise and 1 hour after exercise, and immediately before exercise and 1 hour after exercise for the MOD group were −11.4%, −5.0%, and −15.8%, respectively; those for the HIGH group were −21.5%, 7.9%, and −15.3%, respectively. Limitations Sample size, lack of outcome assessor masking, and physical function measurement subjectivity were limitations. Conclusions Moderate- and high-intensity exercise training, as defined in this study, may lead to similar improvements in physical fitness and physical function in people with type 2 diabetes.

scholarly journals Effect of He Qi San on DNA Methylation in Type 2 Diabetes Mellitus Patients with Phlegm-blood Stasis Syndrome

2019 ◽  
Vol 17 (1) ◽  
pp. 1213-1221
Author(s):  
Chu Shufang ◽  
Zhou Yinan ◽  
Li Huilin ◽  
Zhao Hengxia ◽  
Liu Deliang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Dna Methylation ◽  
Type 2 Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Insulin Signaling ◽  
Blood Stasis ◽  
Blood Stasis Syndrome ◽  
Glucose And Lipid Metabolism

AbstractThis study was performed to elucidate the potential influence of He Qi San (HQS) on glucose and lipid metabolism in type 2 diabetes mellitus (T2DM) patients with phlegm-blood stasis syndrome (PBSS), and to determine DNA methylation changes. Sixty T2DM patients with PBSS were randomly divided into control and HQS groups. The control group received conventional treatments, and the HQS group received conventional treatments plus HQS. Glucose metabolism (FPG, 2hPG, FINS, and HbA1c) and lipid metabolism indexes (TG, TC and LDL-C) were determined. Genes with differential DNA methylation were subjected to GO and KEGG analyses. Glucose and lipid metabolism indexes in both groups were reduced, but were much more pronounced in the HQS group. Differential promoter CpG methylation regions were identified in 682 genes, including 426 genes with high-CpG promoters, 150 genes with intermediate CpG promoters, and 106 genes with low CpG promoters. Genes with differential DNA methylation were mainly enriched in the AMPK and insulin signaling pathways, terpenoid backbone biosynthesis, and renin secretion. We concluded that HQS remarkably improved indexes of glucose and lipid metabolism in T2DM patients with PBSS through regulating the DNA methylation of genes in the AMPK and insulin signaling pathways and terpenoid backbone biosynthesis.

scholarly journals Constitution of a comprehensive phytochemical profile and network pharmacology based investigation to decipher molecular mechanisms of Teucrium polium L. in the treatment of type 2 diabetes mellitus

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10111
Author(s):  
Vahap Murat Kutluay ◽  
Neziha Yagmur Diker
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Signaling Pathway ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Network Pharmacology ◽  
Teucrium Polium ◽  
Phytochemical Profile

Background Type 2 diabetes mellitus (T2DM) is a metabolic disease affecting a huge population worldwide. Teucrium polium L. has been used as a folk medicine for the treatment of T2DM in Anatolia, Turkey. The antihyperglycemic effect of the plant was reported previously. However, there was no detailed study on the underlying molecular mechanisms. In this study, we generated a research plan to clarify the active constituents of the extract and uncover the molecular mechanisms using network pharmacology analysis. Methods For this purpose, we composed a dataset of 126 compounds for the phytochemical profile of the aerial parts of T. polium. Drug-likeness of the compounds was evaluated, and 52 compounds were selected for further investigation. A total of 252 T2DM related targets hit by selected compounds were subjected to DAVID database. Results The KEGG pathway analysis showed enrichment for the TNF signaling pathway, insulin resistance, the HIF-1 signaling pathway, apoptosis, the PI3K-AKT signaling pathway, the FOXO signaling pathway, the insulin signaling pathway, and type 2 diabetes mellitus which are related to T2DM . AKT1, IL6, STAT3, TP53, INS, and VEGFA were found to be key targets in protein-protein interaction. Besides these key targets, with this study the role of GSK3β, GLUT4, and PDX1 were also discussed through literature and considered as important targets in the antidiabetic effect of T. polium. Various compounds of T. polium were shown to interact with the key targets activating PI3K-AKT and insulin signaling pathways. Conclusions According to these findings, mainly phenolic compounds were identified as the active components and IRS1/PI3K/AKT signaling and insulin resistance were identified as the main pathways regulated by T. polium. This study reveals the relationship of the compounds in T. polium with the targets of T2DM in human. Our findings suggested the use of T. polium as an effective herbal drug in the treatment of T2DM and provides new insights for further research on the antidiabetic effect of T. polium.

Type-2 diabetes, a co-morbidity in Covid-19: does insulin signaling matter?

2021 ◽  
Author(s):  
Devanshi Mishra ◽  
Chinmoy Sankar Dey
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Homeostasis ◽  
Cross Talk ◽  
Insulin Signaling ◽  
Clinical Studies ◽  
Scientific Community ◽  
Major Objective ◽  
Glucose Levels ◽  
Co Morbidity

Type-2 Diabetes is associated with one of the co-morbidities due to SARS-Coronavirus 2 (SARS-Cov2) infection. Clinical studies show out of control glucose levels in SARS-Cov2 infected patients with type-2 diabetes. There is no experimental evidence suggesting aberrant molecular pathway(s) that explains why SARS-Cov2 infected patients with type-2 diabetes have uncontrolled glucose homeostasis and are co-morbid. In this article, we have highlighted major proteins involved in SARS-Cov2 infection, like, ACE 2, proteases like, TMPRSS2, Furin and their connectivity to insulin signaling molecules like, PI3K, Akt, AMPK, MAPK, mTOR, those regulate glucose homeostasis and the possible outcome of that cross-talk. We also raised concerns about the effect of anti-SARS-Cov2 drugs on patients with type-2 diabetes with reference to insulin signaling and the outcome of their possible cross-talk. There are no studies to decipher the possibilities of these obvious cross-talks. The major objective of this article is to urge the scientific community to explore the possibility of determining whether derangement of insulin signaling could be one of the possible causes of the patients with type-2 diabetes being co-morbid due to SARS-Cov2 infection.

scholarly journals Association of angiotensinogen and angiotensin II receptor type I polymorphisms with biomarkers of carbohydrate and lipid metabolism in Dagestan residents with type 2 diabetes and hypertension

2021 ◽  
Vol 26 (10) ◽  
pp. 4549
Author(s):  
M. Z. Saidov ◽  
S. N. Mammaev ◽  
G. M. Magadova ◽  
R. M. Balamirzoeva ◽  
Z. Sh. Magomedova ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Angiotensin Ii ◽  
Genetic Polymorphisms ◽  
Type I ◽  
Angiotensin Ii Receptor ◽  
C Peptide ◽  
Glucose Levels ◽  
Carbohydrate And Lipid Metabolism

Aim. To study the associations of angiotensinogen (AGT) (s4762(С521Т), rs699(Т704C)) and angiotensin II receptor type I (AGTR1) (rs5186(A1166C)) genetic polymorphisms with serum levels of insulin, glucagon, C-peptide, leptin, as well as with dyslipidemia and glycemic levels in Dagestan residents with combination of type 2 diabetes (T2D) and hypertension (HTN), as well as with isolated T2D/HTN.Material and methods. We examined 16 patients with isolated T2D, 59 patients with T2D+HTN and 51 patients with isolated HTN from Dagestan. Genetic polymorphisms of the AGT and AGTR1 genes were studied. The levels of insulin, glucagon, C-peptide, and leptin were studied by enzyme-linked immunosorbent assay (ELISA), while lipid and carbohydrate metabolism — by biochemical methods.Results. In patients with T2D, the association of CC genotype of AGT gene rs4762(С521Т) polymorphism with a leptin decrease was determined, while its CT genotype was associated with an increase in serum level of triglycerides. The TC genotype of AGT gene rs699(Т704C) polymorphism was associated with an increase in leptin, triglyceride and glucose levels. The AA genotype of AGTR1 gene rs5186(A1166C) polymorphism was associated with an increase in insulin and glucose levels, as well as a decrease in leptin level. In patients with a combination of T2D and HTN, CC and CT genotypes of AGT gene rs4762(С521Т) polymorphism was associated with a decrease in glucagon level. The TT genotype of AGT gene rs699(Т704C) polymorphism was associated with an increase in insulin, triglyceride, glucose and body mass index (BMI) levels. In isolated HTN, the CC and CT genotypes of AGT gene rs4762(С521Т) polymorphism were associated ith a decrease in glucagon level. The TT genotype of AGT gene rs699(Т704C) polymorphism was associated with increased levels of insulin, low density lipoproteins, and BMI.Conclusion. Associations of AGT (s4762(С521Т), rs699(Т704C)) and AGTR1 (rs5186(A1166C)) genetic polymorphisms with carbohydrate and lipid metabolism changes are an important pathogenetic link of T2D and HTN, which allows developing an individual prognosis of these diseases in Dagestan residents.

scholarly journals Diabetes and Heart Failure: Multi-Omics Approaches

2021 ◽  
Vol 12 ◽  
Author(s):  
Akram Tayanloo-Beik ◽  
Peyvand Parhizkar Roudsari ◽  
Mostafa Rezaei-Tavirani ◽  
Mahmood Biglar ◽  
Ozra Tabatabaei-Malazy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Medical Systems ◽  
Global Issues ◽  
Glucose Levels ◽  
Glycation End Products ◽  
Amplifying Effect

Diabetes and heart failure, as important global issues, cause substantial expenses to countries and medical systems because of the morbidity and mortality rates. Most people with diabetes suffer from type 2 diabetes, which has an amplifying effect on the prevalence and severity of many health problems such as stroke, neuropathy, retinopathy, kidney injuries, and cardiovascular disease. Type 2 diabetes is one of the cornerstones of heart failure, another health epidemic, with 44% prevalence. Therefore, finding and targeting specific molecular and cellular pathways involved in the pathophysiology of each disease, either in diagnosis or treatment, will be beneficial. For diabetic cardiomyopathy, there are several mechanisms through which clinical heart failure is developed; oxidative stress with mediation of reactive oxygen species (ROS), reduced myocardial perfusion due to endothelial dysfunction, autonomic dysfunction, and metabolic changes, such as impaired glucose levels caused by insulin resistance, are the four main mechanisms. In the field of oxidative stress, advanced glycation end products (AGEs), protein kinase C (PKC), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are the key mediators that new omics-driven methods can target. Besides, diabetes can affect myocardial function by impairing calcium (Ca) homeostasis, the mechanism in which reduced protein phosphatase 1 (PP1), sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a), and phosphorylated SERCA2a expressions are the main effectors. This article reviewed the recent omics-driven discoveries in the diagnosis and treatment of type 2 diabetes and heart failure with focus on the common molecular mechanisms.

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