Changes in Glycolipid Metabolism During A High-Sucrose Feeding in Spontaneously Diabetic Torii (SDT) Rats, A Genetic Model of Nonobese Type 2 Diabetes

2010 ◽  
Vol 9 (22) ◽  
pp. 2883-2889 ◽  
Author(s):  
Takeshi Ohta ◽  
Katsuhiro Miyajima ◽  
Takahisa Yamada
Keyword(s):  
Type 2 Diabetes ◽  
Genetic Model ◽  
Glycolipid Metabolism ◽  
Sucrose Feeding ◽  
High Sucrose Feeding ◽  
High Sucrose

scholarly journals Systemic Metabolic Alterations Correlate with Islet-Level Prostaglandin E2 Production and Signaling Mechanisms That Predict β-Cell Dysfunction in a Mouse Model of Type 2 Diabetes

Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 58 ◽  
Author(s):  
Michael D. Schaid ◽  
Yanlong Zhu ◽  
Nicole E. Richardson ◽  
Chinmai Patibandla ◽  
Irene M. Ong ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Prostaglandin E2 ◽  
Genetic Model ◽  
Cell Mass ◽  
Arachidonic Acid Metabolite ◽  
Β Cell ◽  
Human Organ ◽  
Cell Dysfunction ◽  
Primary Mouse

The transition from β-cell compensation to β-cell failure is not well understood. Previous works by our group and others have demonstrated a role for Prostaglandin EP3 receptor (EP3), encoded by the Ptger3 gene, in the loss of functional β-cell mass in Type 2 diabetes (T2D). The primary endogenous EP3 ligand is the arachidonic acid metabolite prostaglandin E2 (PGE2). Expression of the pancreatic islet EP3 and PGE2 synthetic enzymes and/or PGE2 excretion itself have all been shown to be upregulated in primary mouse and human islets isolated from animals or human organ donors with established T2D compared to nondiabetic controls. In this study, we took advantage of a rare and fleeting phenotype in which a subset of Black and Tan BRachyury (BTBR) mice homozygous for the Leptinob/ob mutation—a strong genetic model of T2D—were entirely protected from fasting hyperglycemia even with equal obesity and insulin resistance as their hyperglycemic littermates. Utilizing this model, we found numerous alterations in full-body metabolic parameters in T2D-protected mice (e.g., gut microbiome composition, circulating pancreatic and incretin hormones, and markers of systemic inflammation) that correlate with improvements in EP3-mediated β-cell dysfunction.

SERUM LIPIDS DURING SHORT-TERM HIGH GLUCOSE AND HIGH SUCROSE FEEDING IN INFANTS

PEDIATRICS ◽  
1972 ◽  
Vol 50 (1) ◽  
pp. 84-91
Author(s):  
I. Tamir ◽  
D. Epstein ◽  
D. Heldenberg ◽  
O. Levtow ◽  
B. Werbin
Keyword(s):  
High Glucose ◽  
Caloric Intake ◽  
Serum Triglyceride ◽  
Normal Diet ◽  
Total Serum ◽  
Short Term ◽  
Total Caloric Intake ◽  
Sucrose Feeding ◽  
High Sucrose Feeding ◽  
High Sucrose

The effects of short-term high glucose and high sucrose diets on serum lipids were estimated in six healthy infants aged 4 to 11 months. Each carbohydrate-rich diet was given for 5 days and preceded by 3 days of a "normal" diet. During the high CHO feeding, sucrose or glucose supplied 73% of the total caloric intake, while on the "normal" diet only 40% for the total caloric intake was derived from CHO (glucose only). The percentage of total caloric intake supplied by protein was almost identical in the three diets used. An increase in serum triglyceride (TG) concentration, of almost equal magnitude, was seen following both high CHO feeding periods. Upon resumption of the "normal" diet, serum TG concentrations approached initial concentrations. No consistent changes occurred in total serum cholesterol concentrations or in total serum phospholipid concentrations. A significant increase in the percentage concentration of palmitoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This increase was slightly but not significantly greater following high sucrose feeding. A significant decrease in the percentage concentration of linoleic acid of serum triglyceride fatty acids occurred on both high CHO diets. This decrease was slightly but not significantly greater following high sucrose feeding. Therefore, it seems that on a short-term basis, high sucrose and high glucose feeding, in healthy infants, will result in similar changes in serum triglyceride concentrations and serum triglyceride fatty acid patterns.

scholarly journals miR-125a-5p ameliorates hepatic glycolipid metabolism disorder in type 2 diabetes mellitus through targeting of STAT3

Theranostics ◽  
2018 ◽  
Vol 8 (20) ◽  
pp. 5593-5609 ◽  
Author(s):  
Lina Xu ◽  
Yue Li ◽  
Lianhong Yin ◽  
Yan Qi ◽  
Huijun Sun ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

Glycolipid metabolism and liver transcriptomic analysis of the therapeutic effects of pressed degreased walnut meal extracts on type 2 diabetes mellitus rats

2020 ◽  
Vol 11 (6) ◽  
pp. 5538-5552 ◽  
Author(s):  
Yulan Li ◽  
Dan Chen ◽  
Chengmei Xu ◽  
Qingyujing Zhao ◽  
Yage Ma ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Transcriptomic Analysis ◽  
Therapeutic Effects ◽  
Glycolipid Metabolism

WMP (extract of pressed degreased walnut meal) is rich in polyphenols which exhibit multiple therapeutic effects.

scholarly journals Association of KCNQ1rs2237892C ⟶ T Gene with Type 2 Diabetes Mellitus: A Meta-Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Wen-Jia Han ◽  
Jian-Yi Deng ◽  
Hua Jin ◽  
Li-Ping Yin ◽  
Jin-Xia Yang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gene Polymorphism ◽  
Genetic Model ◽  
Meta Analysis ◽  
High Morbidity ◽  
Genome Wide Association Studies ◽  
Asian Populations

Background. Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases in adults, causing high morbidity and mortality worldwide. In recent years, the prevalence of T2DM has been increasing significantly, and genome-wide association studies (GWAS) have shown that KCNQ1 significantly increases the risk of T2DM. Objective. To find large-scale evidence on whether the KCNQ1rs2237892C⟶T gene polymorphism is associated with T2DM susceptibility. Methods. A comprehensive review of the Chinese and English literature on the association of T2DM with KCNQ1rs2237892 is published by PubMed and Baidu Academic. The included literature was part or all of the studied loci which were evaluated for association with T2DM. Forest plots were made of the included literature to analyze the association of KCNQ1 with polymorphisms of the studied loci, and funnel plots and Egger’s test were used to evaluate the publication bias of the selected included literature. Results. Ten case-control studies including a total of 7027 cases and 8208 controls met our inclusion criteria. Allele (C allele frequency distribution) (OR: 1.19; 95% CI: 0.87,1.62; P < 0.00001 ), recessive (OR: 0.73; 95% CI: 0.45,1.18; P < 0.00001 ) genetic model under the full population was observed between KCNQ1rs2237892C⟶T gene polymorphism and T2DM without a significant relationship. In a stratified analysis by race, a meaningful association was found in non-Asian populations under the allelic genetic model, but no association was found in Asian populations. Conclusion. This meta-analysis showed no significant association between the rs2237892 polymorphism of the KCNQ1 gene and the risk of T2DM.

P1-152 - High sucrose feeding-induced abnormalities of neuronal NO synthase in rat pancreatic bêta-cells and skeletal muscle

2006 ◽  
Vol 67 (5) ◽  
pp. 460-461
Author(s):  
K. Mezghenna ◽  
S. Péraldi-Roux ◽  
G. Dubois ◽  
M. Manteghetti ◽  
M. Tournier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
No Synthase ◽  
Neuronal No Synthase ◽  
Sucrose Feeding ◽  
High Sucrose Feeding ◽  
High Sucrose

scholarly journals Physical Exercise as Therapy for Type 2 Diabetes Mellitus: From Mechanism to Orientation

2019 ◽  
Vol 74 (4) ◽  
pp. 313-321 ◽  
Author(s):  
Dan Yang ◽  
Yifan Yang ◽  
Yanlin Li ◽  
Rui Han
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Therapy ◽  
Metabolic Diseases ◽  
Whole Body ◽  
Mechanism Study ◽  
Physiological Mechanisms ◽  
Glycolipid Metabolism ◽  
Randomized Controlled Studies

Background: Exercise therapy plays an important role in the prevention and treatment of type 2 diabetes (T2DM). The mechanism of exercise therapy in the improvement of glycolipid metabolism of T2DM is very complex and not completely clear. Summary: Exercise training improves the whole body metabolic health in patients with T2DM, leading to an increase in glycolipid uptake and utilization, improved insulin sensitivity, optimized body mass index, and modulated DNA methylation, etc. Recent findings support that some cytokines such as irisin, osteocalcin, and adiponectin are closely related to exercise and metabolic diseases. This study briefly reviews the physiological mechanisms of exercise therapy in diabetes and the potential role of these cytokines in exercise. Key Messages: More high-quality, targeted, randomized controlled studies are needed urgently, from mechanism study to treatment direction, to provide a more theoretical basis for exercise therapy and to explore new therapeutic targets for diabetes.

scholarly journals Association of miR-146a polymorphism rs2910164 and type 2 diabetes risk: a meta-analysis

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052093131
Author(s):  
Liqing Cheng ◽  
Min Zhou ◽  
Dongmei Zhang ◽  
Bing Chen
Keyword(s):  
Type 2 Diabetes ◽  
Gene Polymorphisms ◽  
Disease Duration ◽  
Genetic Model ◽  
Meta Analysis ◽  
Confounding Factors ◽  
Dominant Model ◽  
Subgroup Analyses

Objective Circulating miR-146a is aberrantly expressed in patients with type 2 diabetes (T2D), probably resulting from gene polymorphisms. However, the role of polymorphism rs2910164 in T2D pathogenesis remains controversial. Thus, we designed a meta-analysis to investigate the association between rs2910164 and T2D. Methods PubMed and Embase were searched for eligible papers in English published through September 2, 2019. Random or fixed effect models were used to determine risk estimates according to heterogeneities. Results Four studies, involving 2,069 patients and 1,950 controls, were included. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to pool the effect size. The pooled ORs and 95% CIs were 1.501 (0.887–2.541), 1.102 (0.931–1.304), 1.276 (0.900–1.811), 1.204 (0.878–1.652), 1.238 (0.880–1.740), and 1.350 (0.904–2.016) under the homozygote, heterozygote (CG vs. GG and CC vs. CG), dominant, allele, and recessive models, respectively. Heterogeneity was detected in most genetic models, with subgroup analyses performed by ethnicity, genotyping method, and disease duration. The co-dominant model was determined to be the most appropriate genetic model. Conclusions Our findings suggested that polymorphism rs2910164 is not correlated with T2D susceptibility. However, the results should be interpreted with caution because of confounding factors.

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