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Mechanisms of diabetes from acute pancreatitis in African Americans and Hispanics

非裔美国人和西班牙裔人急性胰腺炎导致糖尿病的机制

基本信息

批准号：
10461069
负责人：
Brian Thomas Layden
金额：
$ 24.06万
依托单位：
UNIVERSITY OF ILLINOIS AT CHICAGO
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-17 至 2025-07-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10461069
关键词：
African American African American population Animals Autoimmune B-Lymphocytes Bacteria Cell physiology Chicago Clinical Consumption Country County Data Data Set Development Diabetes Mellitus Diet Dietary Fiber Disease Endocrine Energy-Generating Resources Environment Environmental Risk Factor Etiology Fatty acid glycerol esters Feces Fiber General Population Generations Genes Goals Health Disparities Research Hispanic Hispanic Populations Hydrogen Sulfide Immunologics Individual Inflammatory Injury Insulin Resistance Insulin-Dependent Diabetes Mellitus Intake Lead Link Longitudinal cohort Measures Meat Mediating Mediation Metabolic Minority Groups Modeling Morbidity - disease rate Nature Non-Insulin-Dependent Diabetes Mellitus Not Hispanic or Latino Nutrient Pancreatitis Pathway interactions Patients Population Heterogeneity Prevention strategy Production Proteins Risk Risk Factors Role Sampling Serum Sulfur Metabolism Pathway Sum Time Translations United States Volatile Fatty Acids acute pancreatitis base clinical center cohort cooking defined contribution diabetes risk dietary ethnic diversity gut microbiome gut microbiota health disparity high risk immunoregulation improved in vivo Model member microbial microbiome mortality multidisciplinary novel novel marker patient population racial diversity treatment strategy

项目摘要

Mechanisms of diabetes from acute pancreatitis in African Americans and Hispanics Acute pancreatitis (AP) leads to oxidative and inflammatory injury, ensuing parenchymal damage, exocrine and/or endocrine insufficiencies including the development of diabetes. While AP increases the risk of the development of diabetes, the type of diabetes, either type 1 diabetes (T1D, autoimmune) as compared to other forms of diabetes, is not clear. Considering diabetes is a major health disparity in our country, understanding AP-driven diabetes is needed in racially diverse populations. Additionally, the risk factors or the mechanisms lead to AP driven diabetes is also unclear. Importantly, the gut microbiota is a novel factor linked to the genesis of both T1D and type 2 diabetes (T2D), yet its role in AP driven diabetes is not known. Moreover, in our diverse patient population, the compositional profiles of gut microbiota are not well defined. Our proposal leverages our extensive, multiple institutional, cohort of patients which is predominantly African American (AA) and Hispanic and our broad, multidiscplinary team with a range of expertise in clinical pancreatology and diabetes, gut microbiome, diet and health disparities research. In sum, the goal of our proposal is three-fold: 1) to define in our diverse patient population that is predominantly AA and Hispanic, the relationship between AP to T1D, and other forms of diabetes, and the factors associated with development of diabetes, and to mechanistically define 2) how diet, specifically enriched in animal protein and fat (DH-APF), through its interaction with the gut microbiota, impacts AP-driven diabetes, and 3) how fiber from the diet, through the generation of short chain fatty acids (SCFAs), a recently recognized factor identified in the genesis of T1D and T2D, mediates AP-driven T1D.

非裔美国人和西班牙裔美国人急性胰腺炎引起糖尿病的机制