scholarly journals Genetic Variance inUncoupling Protein 2in Relation to Obesity, Type 2 Diabetes, and Related Metabolic Traits: Focus on the Functional −866G>A Promoter Variant (rs659366)

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Louise T. Dalgaard
Keyword(s):  
Type 2 Diabetes ◽  
Candidate Gene ◽  
Transcription Initiation ◽  
Current Evidence ◽  
Inner Mitochondrial Membrane ◽  
Obesity And Diabetes ◽  
Atp Generation ◽  
Glucose Stimulated Insulin Secretion

Uncoupling proteins (UCPs) are mitochondrial proteins able to dissipate the proton gradient of the inner mitochondrial membrane when activated. This decreases ATP-generation through oxidation of fuels and may theoretically decrease energy expenditure leading to obesity. Evidence fromUcp(−/−)mice revealed a role of UCP2 in the pancreaticβ-cell, becauseβ-cells without UCP2 had increased glucose-stimulated insulin secretion. Thus, from being a candidate gene for obesity UCP2 became a valid candidate gene for type 2 diabetes mellitus. This prompted a series of studies of the human UCP2 and UCP3 genes with respect to obesity and diabetes. Of special interest was a promoter variant of UCP2 situated 866bp upstream of transcription initiation (−866G>A, rs659366). This variant changes promoter activity and has been associated with obesity and/or type 2 diabetes in several, although not all, studies. The aim of the current paper is to summarize current evidence of association of UCP2 genetic variation with obesity and type 2 diabetes, with focus on the −866G>A polymorphism.

scholarly journals Quinoa’s Potential to Enhance Dietary Management of Obesity and Type-2 Diabetes: A Review of the Current Evidence

Diabetology ◽  
2021 ◽  
Vol 2 (2) ◽  
pp. 77-94
Author(s):  
Alexander Little ◽  
Kevin Murphy ◽  
Patrick Solverson
Keyword(s):  
Type 2 Diabetes ◽  
Best Management Practices ◽  
Management Practices ◽  
The United States ◽  
Lipid Absorption ◽  
Current Evidence ◽  
Future Research ◽  
Dietary Management ◽  
Obesity And Diabetes

The prevalence of diet-induced obesity and type-2 diabetes remains a growing concern in the United States. As best management practices still include improved diet and physical activity, bioactive food components, contained within functional foods, show promise in curbing the cardiometabolic complications associated with excess weight and diabetes. Quinoa is an emerging candidate crop for its versatility in wide-ranging growing conditions as one approach to address food security, but it also contains several components that may serve as a dietary tool for post-industrial countries struggling with the health complications of caloric excess. Preliminary rodent feeding studies demonstrate that components within quinoa, namely, phytosteroids, phenolics, polysaccharides, and peptides, can prevent adiposity, dyslipidemia, and hyperglycemia. Mechanistic activity may involve reduced lipid absorption and adipogenesis, increased energy expenditure and glucose oxidation and corrected gut microbiota. Other intestinal actions may include blocked carbohydrate digestion with enhanced incretin signaling. Evidence in clinical trials is lacking and future research spanning cells to the clinic is needed to further elucidate the interesting preliminary reports reviewed here. Quinoa offers several unique attributes that could be harnessed to improve the dietary management of obesity and diabetes.

scholarly journals Role of folate in nonalcoholic fatty liver disease

2017 ◽  
Vol 95 (10) ◽  
pp. 1141-1148 ◽  
Author(s):  
Victoria Sid ◽  
Yaw L. Siow ◽  
Karmin O
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Serum Folate ◽  
Nonalcoholic Fatty Liver ◽  
Obesity And Diabetes

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of chronic liver conditions that are characterized by steatosis, inflammation, fibrosis, and liver injury. The global prevalence of NAFLD is rapidly increasing in proportion to the rising incidence of obesity and type 2 diabetes. Because NAFLD is a multifaceted disorder with many underlying metabolic abnormalities, currently, there is no pharmacological agent that is therapeutically approved for the treatment of this disease. Folate is a water-soluble B vitamin that plays an essential role in one-carbon transfer reactions involved in nucleic acid biosynthesis, methylation reactions, and sulfur-containing amino acid metabolism. The liver is the primary organ responsible for storage and metabolism of folates. Low serum folate levels have been observed in patients with obesity and diabetes. It has been reported that a low level of endogenous folates in rodents perturbs folate-dependent one-carbon metabolism, and may be associated with development of metabolic diseases such as NAFLD. This review highlights the biological role of folate in the progression of NAFLD and its associated metabolic complications including obesity and type 2 diabetes. Understanding the role of folate in metabolic disease may position this vitamin as a potential therapeutic for NAFLD.

Current evidence for a role of GLP-1 in Roux-en-Y gastric bypass-induced remission of type 2 diabetes

2011 ◽  
Vol 14 (4) ◽  
pp. 291-298 ◽  
Author(s):  
N. A. Rhee ◽  
T. Vilsbøll ◽  
F. K. Knop
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Current Evidence

scholarly journals In vivo phosphoproteomics reveals pathogenic signaling changes in diabetic islets

2018 ◽  
Author(s):  
Francesca Sacco ◽  
Anett Seelig ◽  
Sean J. Humphrey ◽  
Natalie Krahmer ◽  
Francesco Volta ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Drug Targets ◽  
High Sensitivity ◽  
Glucose Stimulated Insulin Secretion

SUMMARYProgressive decline of pancreatic beta cells function is key to the pathogenesis of type 2 diabetes. Protein phosphorylation is the central mechanism controlling glucose-stimulated insulin secretion in beta cells. However, if and how signaling networks are remodeled in diabetic isletsin vivoremain unknowns. Here we applied high-sensitivity mass spectrometry-based proteomics and quantified the levels of about 6,500 proteins and 13,000 phosphopeptides in islets of obese diabetic mice and matched controls. This highlighted drastic remodeling of key kinase hubs and signaling pathways. We integrated our phosphoproteomic dataset with a literature-derived signaling network, which revealed a crucial and conserved role of GSK3 kinase in the control of the beta cells-specific transcription factor PDX1 and insulin secretion, which we functionally verified. Our resource will enable the community to investigate potential mechanisms and drug targets in type 2 diabetes.

scholarly journals The Role of Endogenous Incretin Secretion as Amplifier of Glucose-Stimulated Insulin Secretion in Healthy Subjects and Patients With Type 2 Diabetes

Diabetes ◽  
2012 ◽  
Vol 61 (9) ◽  
pp. 2349-2358 ◽  
Author(s):  
H. J. Woerle ◽  
L. Carneiro ◽  
A. Derani ◽  
B. Goke ◽  
J. Schirra
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Healthy Subjects ◽  
Incretin Secretion ◽  
Glucose Stimulated Insulin Secretion

scholarly journals The Role of Sleep Curtailment on Leptin Levels in Obesity and Diabetes Mellitus

Obesity Facts ◽  
2021 ◽  
Vol 14 (2) ◽  
pp. 214-221
Author(s):  
Maryam Mosavat ◽  
Mitra Mirsanjari ◽  
Diana Arabiat ◽  
Aisling Smyth ◽  
Lisa Whitehead
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Food Intake ◽  
Sleep Deprivation ◽  
Sleep Duration ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Obesity And Diabetes

Emerging evidence has identified sleep as a significant, but modifiable, risk factor for metabolic syndrome, diabetes, and obesity. Leptin, an adipocyte-derived peptide and a regulator of food intake and energy expenditure, has been shown to be associated with a short sleep duration in the pathophysiology of obesity and consequently type 2 diabetes. This review focuses on the current evidence indicating the effects of a short sleep duration on the regulation of leptin concentration in association with obesity and diabetes mellitus. In summary, the evidence suggests that sleep deprivation, by affecting leptin regulation, may lead to obesity and consequently development of type 2 diabetes through increased appetite and food intake. However, findings on the role of leptin in diabetes due to sleep deprivation are contradictory, and further studies with larger sample sizes are needed to confirm previous findings.

High prevalence of lower extremity peripheral artery disease in type 2 diabetes patients with diabetic nephropathy and the role of netrin-1 levels

2017 ◽  
Author(s):  
Ahmet Kor ◽  
Suleyman Baldane ◽  
Suleyman Hilmi Ipekci ◽  
Kamile Marakoglu ◽  
Ali Altinok ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Lower Extremity ◽  
Peripheral Artery Disease ◽  
Peripheral Artery ◽  
High Prevalence ◽  
Artery Disease ◽  
Diabetes Patients

The role of oncostatin m in the development of type 2 diabetes associated with obesity

2018 ◽  
Author(s):  
Siri Taxeras ◽  
Irene Piquer-Garcia ◽  
Silvia Pellitero ◽  
Rocio Puig ◽  
Eva Martinez ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oncostatin M
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