scholarly journals Behavioral Strategies to Lower Postprandial Glucose in Those with Type 2 Diabetes May Also Lower Risk of Coronary Heart Disease

2018 ◽  
Vol 10 (1) ◽  
pp. 277-281 ◽  
Author(s):  
Daniel J. Cox ◽  
Kun Fang ◽  
Anthony L. McCall ◽  
Mark R. Conaway ◽  
Tom A. Banton ◽  
...  
Author(s):  
Qin Wang ◽  
Clare Oliver-Williams ◽  
Olli T Raitakari ◽  
Jorma Viikari ◽  
Terho Lehtimäki ◽  
...  

Abstract Aims  Angiopoietin-like protein 3 (ANGPTL3) and 4 (ANGPTL4) inhibit lipoprotein lipase (LPL) and represent emerging drug targets to lower circulating triglycerides and reduce cardiovascular risk. To investigate the molecular effects of genetic mimicry of ANGPTL3 and ANGPTL4 inhibition and compare them to the effects of genetic mimicry of LPL enhancement. Methods and results  Associations of genetic variants in ANGPTL3 (rs11207977-T), ANGPTL4 (rs116843064-A), and LPL (rs115849089-A) with an extensive serum lipid and metabolite profile (208 measures) were characterized in six cohorts of up to 61 240 participants. Genetic associations with anthropometric measures, glucose-insulin metabolism, blood pressure, markers of kidney function, and cardiometabolic endpoints via genome-wide summary data were also explored. ANGPTL4 rs116843064-A and LPL rs115849089-A displayed a strikingly similar pattern of associations across the lipoprotein and lipid measures. However, the corresponding associations with ANGPTL3 rs11207977-T differed, including those for low-density lipoprotein and high-density lipoprotein particle concentrations and compositions. All three genotypes associated with lower concentrations of an inflammatory biomarker glycoprotein acetyls and genetic mimicry of ANGPTL3 inhibition and LPL enhancement were also associated with lower C-reactive protein. Genetic mimicry of ANGPTL4 inhibition and LPL enhancement were associated with a lower waist-to-hip ratio, improved insulin-glucose metabolism, and lower risk of coronary heart disease and type 2 diabetes, whilst genetic mimicry of ANGPTL3 was associated with improved kidney function. Conclusions  Genetic mimicry of ANGPTL4 inhibition and LPL enhancement have very similar systemic metabolic effects, whereas genetic mimicry of ANGPTL3 inhibition showed differing metabolic effects, suggesting potential involvement of pathways independent of LPL. Genetic mimicry of ANGPTL4 inhibition and LPL enhancement were associated with a lower risk of coronary heart disease and type 2 diabetes. These findings reinforce evidence that enhancing LPL activity (either directly or via upstream effects) through pharmacological approaches is likely to yield benefits to human health.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2436-PUB
Author(s):  
SHISHI XU ◽  
CHARLES A. SCOTT ◽  
RUTH L. COLEMAN ◽  
JAAKKO TUOMILEHTO ◽  
RURY R. HOLMAN

2020 ◽  
Vol 26 ◽  
Author(s):  
Margarita A. Sazonova ◽  
Anastasia I. Ryzhkova ◽  
Vasily V. Sinyov ◽  
Marina D. Sazonova ◽  
Tatiana V. Kirichenko ◽  
...  

Background: The present review article considers some chronic diseases of vascular and metabolic genesis, the causes of which may be mitochondrial dysfunction. Very often, in the long course of the disease, complications may occur, leading to myocardial infarction or ischemic stroke and as a result, death.In particular, a large percentage of human deaths nowadays belongs to cardiovascular diseases such as coronary heart disease (CHD), arterial hypertension, cardiomyopathies and type 2 diabetes mellitus. Objective: The aim of the present review was the analysis of literature sources, devoted to an investigation of a link of mitochondrial DNA mutations with chronic diseases of vascular and metabolic genesis, Results: The analysis of literature indicates the association of the mitochondrial genome mutations with coronary heart disease, type 2 diabetes mellitus, hypertension and various types of cardiomyopathies. Conclusion: The detected mutations can be used to analyze the predisposition to chronic diseases of vascular and metabolic genesis. They can also be used to create molecular-cell models necessary to evaluate the effectiveness of drugs developed for treatment of these pathologies. MtDNA mutations associated withthe absence of diseases of vascular and metabolic genesis could be potential candidates for gene therapy of diseases of vascular and metabolic genesis.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Elena M. Yubero-Serrano ◽  
Juan F. Alcalá-Diaz ◽  
Francisco M. Gutierrez-Mariscal ◽  
Antonio P. Arenas-de Larriva ◽  
Patricia J. Peña-Orihuela ◽  
...  

An amendment to this paper has been published and can be accessed via the original article.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yasunari Yamashita ◽  
Rina Kitajima ◽  
Kiyoshi Matsubara ◽  
Gaku Inoue ◽  
Hajime Matsubara

Abstract Objective In 2018, we conducted a retrospective survey using the medical records of 484 patients with type 2 diabetes. The observed value of coronary heart disease (CHD) incidence after 5 years and the predicted value by the JJ risk engine as of 2013 were compared and verified using the discrimination and calibration values. Results Among the total cases analyzed, the C-statistic was 0.588, and the calibration was p < 0.05; thus, the JJ risk engine could not correctly predict the risk of CHD. However, in the group expected to have a low frequency of hypoglycemia, the C-statistic was 0.646; the predictability of the JJ risk engine was relatively accurate. Therefore, it is difficult to accurately predict the complication rate of patients using the JJ risk engine based on the diabetes treatment policy after the Kumamoto Declaration 2013. The JJ risk engine has several input items (variables), and it is difficult to satisfy them all unless the environment is well-equipped with testing facilities, such as a university hospital. Therefore, it is necessary to create a new risk engine that requires fewer input items than the JJ risk engine and is applicable to several patients.


2018 ◽  
Vol 12 ◽  
pp. 146-157 ◽  
Author(s):  
Rosa Jiménez-Lucena ◽  
Oriol Alberto Rangel-Zúñiga ◽  
Juan Francisco Alcalá-Díaz ◽  
Javier López-Moreno ◽  
Irene Roncero-Ramos ◽  
...  

JAMA ◽  
2013 ◽  
Vol 310 (8) ◽  
pp. 821 ◽  
Author(s):  
Lu Qi ◽  
Qibin Qi ◽  
Sabrina Prudente ◽  
Christine Mendonca ◽  
Francesco Andreozzi ◽  
...  

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