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16,300 grants matching “fatty liver disease”
A Randomized Trial to Compare Surgical and Medical Treatments for Type 2 Diabetes
$500,000Anita P Courcoulas · University Of Pittsburgh At Pittsburgh · RC1 · FY2009 · DK
Genome-wide epigenetic control of circadian metabolism by heme receptor Rev-erb
$500,000Mitchell A. Lazar · University Of Pennsylvania · RC1 · FY2009 · DK
Improving Diagnostic Safety through STeatosis Identification, Risk stratification, and Referral in the ED (STIRRED)
$500,000Amy V Kontrick · Northwestern University At Chicago · R01 · FY2023 · HS
Ubiquitin D as a potential therapeutic target for NASH, HCC and chronic kidney diseases
$500,000Debanjan Dhar · Sanford Burnham Prebys Medical Discovery Institute · R01 · FY2025 · DK
**AWARDS ISSUED PRIOR TO JANUARY 20, 2025, WERE FUNDED UNDER PREVIOUS ADMINISTRATIONS AND MAY NOT REFLECT THE PRIORITIES AND POLICIES OF THE CURRENT ADMINISTRATION.** DURING EMBRYONIC-TO-POST-HATCH TRANSITION IN CHICKEN, THERE IS A DRAMATIC METABOLIC SWITCH FROM, THE EMBRYO DERIVING OVER 90% OF ENERGY FROM YOLK-LIPID OXIDATION TO, THE NEONATAL CHICK LIVER UPREGULATING NEW LIPID SYNTHESIS (LIPOGENESIS). INTERESTINGLY, A SIMILAR METABOLIC MILIEU IS EVIDENT IN FATTY LIVER HEMORRHAGIC SYNDROME (FLHS) IN POULTRY LAYERS AND NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) IN MICE AND HUMANS, BUT ALONG WITH THE TOXIC EFFECTS OF OXIDATIVE STRESS AND INFLAMMATION. INEFFICIENT EMBRYONIC-TO-POST-HATCH TRANSITION IS ALSO A SIGNIFICANT SOURCE OF MORTALITY AND ECONOMIC LOSS TO THE POULTRY INDUSTRY. WE HYPOTHESIZE THAT THE OPTIMAL RELATIONSHIP BETWEEN MITOCHONDRIAL LIPID-OXIDATION AND LIPOGENESIS IN THE LIVER CONTRIBUTES TO THE HEALTHY EMBRYONIC-TO-POST-HATCH SWITCH. DISRUPTING THIS RELATIONSHIP WILL RESULT IN SYMPTOMS OF FATTY LIVER DISEASE, IN TURN LEADING TO INEFFICIENT EMBRYONIC-TO-POST-HATCH TRANSITION AND LOSSES IN PRODUCTIVITY. OUR OBJECTIVE 1 WILL CHARACTERIZE THE ADAPTABILITY OF THE CENTRAL MITOCHONDRIAL NETWORKS AND LIPOGENESIS IN THE LIVER DURING EMBRYONIC-TO-POST-HATCH TRANSITION. OBJECTIVE 2 WILL TEST THE HYPOTHESIS THAT THE MAL-ADAPTABILITY OF THE HEPATIC MITOCHONDRIAL METABOLIC NETWORKS CONTRIBUTE TO METABOLIC DYSFUNCTION IN SMALL-EGG DERIVED EMBRYOS AND CHICKS FROM YOUNGER FLOCKS, COMPARED TO THEIR LARGER AND OLDER COUNTERPARTS. HERE, WE ALSO HYPOTHESIZE THAT BRANCHED CHAIN AMINO ACIDS (BCAAS) WILL POSITIVELY IMPACT THE REMODELING OF MITOCHONDRIAL LIPID METABOLISM AND LIPOGENESIS. THE INVESTIGATION OF THE ROLE OF BCAAS IS UNDER THE PREMISE THAT BCAAS CLOSELY INTERACT WITH AND REGULATE SEVERAL ASPECTS OF MITOCHONDRIAL LIPID METABOLISM. TOWARDS THESE OBJECTIVES, WE WILL INTEGRATE METABOLIC PROFILING BY STATE-OF-THE-ART TECHNIQUES IN STABLE ISOTOPE-BASED MASS SPECTROMETRY (MS) AND NUCLEAR MAGNETIC RESONANCE (NMR), WITH GENE PROFILES FROM RNA-SEQUENCING. THIS STRATEGY WILL HELP US IDENTIFY CENTRAL MECHANISMS PROMOTING THE OPTIMAL CROSSTALK BETWEEN MITOCHONDRIAL FUNCTION, LIPOGENESIS AND HEPATO-CELLULAR STRESS. THIS IN TURN WILL HELP FORMULATE NUTRITIONAL, HORMONAL OR GENETIC STRATEGIES TO OPTIMIZE THE HATCHLING HEALTH. THE IMPACT OF THESE STUDIES WILL BE TOWARDS TARGETING MITOCHONDRIAL FUNCTION AS A NEW PARADIGM TO IMPROVE POULTRY PRODUCTION AND ECONOMICS, SPECIFICALLY BY A) OPTIMIZING THE METABOLIC HEALTH OF THE EMBRYONIC AND HATCHLING LIVER, B) IDENTIFYING METABOLIC MECHANISMS WHICH CAN HELP PREVENT THE ONSET OF FATTY LIVER SYNDROMES.
$500,000University Of Maryland, College Park · · FY2021 · National Institute of Food and Agriculture
NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD) IS THE LEADING CAUSE OF LIVER DISEASE IN ADOLESCENTS AND ADULTS IN THE US AND WORLD, AND ITS RISK HAS INCREASED WITH THE RISE OF OBESITY. USING THE OBESE ZUCKER RAT MODEL, WE PREVIOUSLY REPORTED THAT CONSUMPTION OF SOY PROTEIN DIET REDUCED FATTY LIVER. WE HYPOTHESIZE THAT A SOY PROTEIN DIET WITH HIGH ISOFLAVONE CONTENT COMPARED TO A SOY PROTEIN DIET WITH LOWISOFLAVONE CONTENT WILL 1) REDUCE DEVELOPMENT OF OBESITY-RELATED NAFLD IN YOUNG (ADOLESCENT MODEL) AND ADULT OBESE ZUCKER RATS IN PART BY ALTERING GUT MICROBIOTA AND 2) REVERSE DAMAGE TO LIVER CELLS IN OBESE ZUCKER RATS WITH ESTABLISHED NAFLD IN PART THROUGH GUT MICROBIOTA ALTERATIONS. THE PROPOSAL FOCUSES ON 1) INVESTIGATING THE ROLE OF SOY DIETS AND GUT MICROBIOTA ON PROTECTION FROM NAFLD IN ADOLESCENT AND ADULT RAT MODELS, 2) DETERMINING FOR THE FIRST TIME IF SOY DIETS AND GUTBACTERIAALTERATIONS CAN REVERSE OBESITY-RELATED NAFLD IN THESE MODELS, AND 3) DETERMINING THE EFFECTS OF SOY PROTEIN DIET ON LIVER DAMAGE AND INFLAMMATION MARKERS IN THESE MODELS. WE WILL USE STATE-OF-THE-ART METAGENOMICS AND METAPROTEOMICS TO IDENTIFY THE POPULATION OF GUT MICROORGANISMS AS WELL AS THE FUNCTIONAL BACTERIAL PROTEINS PRESENT. ANALYSIS OF THE MICROBIOTA WILL GENERATE NOVEL DATA ON THE INTERACTION OF OBESITY, SOY PROTEIN DIETS, AND INTESTINAL MICROBIOTA, AND THE POSSIBLE LINK TO PROTECTION FROM NAFLD.
$500,000Arkansas Children'S Research Institute · · FY2020 · National Institute of Food and Agriculture
**AWARDS ISSUED PRIOR TO JANUARY 20, 2025, WERE FUNDED UNDER PREVIOUS ADMINISTRATIONS AND MAY NOT REFLECT THE PRIORITIES AND POLICIES OF THE CURRENT ADMINISTRATION.** FATTY LIVER IS ONE OF THE MOST COMPLEX METABOLIC DISEASE THAT COMMONLY OCCUR IN DAIRY CATTLE WITHIN FEW WEEKS AFTER COWS GIVE BIRTH. COWS WITH FATTY LIVER HAVE IMPAIRED HEALTH, MILK PRODUCTION, AND PROFITABILITY. OUR CENTRAL HYPOTHESIS IS THAT BRANCHED CHAIN AMINO ACIDS (BCAA) OR BRANCHED CHAIN KETOACIDS (BCKA) SUPPLEMENTATION CAN IMPROVE LIVER FUNCTION AND DECREASE INCIDENCE OF FATTY LIVER IN DAIRY COWS. TO EVALUATE THIS HYPOTHESIS, WE WILL TEST THE EXTENT TO WHICH INFUSION OF BCAA AND BCKA INTO BLOOD CIRCULATION DECREASES FAT ACCUMULATION IN THE LIVER. SECONDLY, WE WILL ASSESS WHETHER GENES/ENZYMES REGULATING FAT ACCUMULATION IN THE LIVER RESPOND TO BCAA AND BCKA INFUSION. FINALLY, WE WILL ASSESS KEY METABOLITES REGULATING CELL DEATH IN LIVER OF DAIRY COWS IN EARLY LACTATION. KNOWLEDGE GENERATED FROM THIS PROJECT WILL PROVIDE URGENTLY NEEDED INSIGHT INTO A NOVEL NUTRITIONAL PREVENTATIVE STRATEGY THAT COULD POTENTIALLY BENEFIT BOTH PROFITABILITY AND SUSTAINABILITY OF DAIRY INDUSTRY BY EFFECTIVELY DECREASING PREVALENCE OF FATTY LIVER DURING EARLY LACTATION.
$500,000Michigan State University · · FY2021 · National Institute of Food and Agriculture
Novel Modulators of LDL Metabolism
$500,000Nabil A Elshourbagy · Shifa Biomedical Corporation · R44 · FY2014 · HL
Hyperpolarized C-13 Diffusion MRI Measures of Cellular Transport and Metabolism
$500,000Peder Eric Zufall Larson · University Of California, San Francisco · R01 · FY2017 · EB
Ubiquitin D as a potential therapeutic target for NASH, HCC and chronic kidney diseases
$500,000Debanjan Dhar · University Of California, San Diego · R01 · FY2023 · DK
Hyperpolarized C-13 Diffusion MRI Measures of Cellular Transport and Metabolism
$500,000Peder Eric Zufall Larson · University Of California, San Francisco · R01 · FY2014 · EB
A Randomized Trial to Compare Surgical and Medical Treatments for Type 2 Diabetes
$500,000Anita P Courcoulas · University Of Pittsburgh At Pittsburgh · RC1 · FY2010 · DK
Genome-wide epigenetic control of circadian metabolism by heme receptor Rev-erb
$500,000Mitchell A. Lazar · University Of Pennsylvania · RC1 · FY2010 · DK
Hyperpolarized C-13 Diffusion MRI Measures of Cellular Transport and Metabolism
$500,000Peder Eric Zufall Larson · University Of California, San Francisco · R01 · FY2016 · EB
Dissecting Adipose Depot-Selective Regulation of Gene Programs
$500,000Philipp E Scherer · Ut Southwestern Medical Center · RC1 · FY2010 · DK
Regulation of Alcohol-induced Fatty Liver Disease by Lipid Droplet Trafficking
$499,999Carol A Casey · University Of Nebraska Medical Center · RC1 · FY2009 · AA
Them1 Inhibitors for the Management of Non-Alcoholic Fatty Liver Disease
$499,999David E Cohen · Brigham And Women'S Hospital · R01 · FY2025 · DK
Them1 Inhibitors for the Management of Non-Alcoholic Fatty Liver Disease
$499,999David E Cohen · Brigham And Women'S Hospital · R01 · FY2023 · DK
Dissecting Adipose Depot-Selective Regulation of Gene Programs
$499,998Philipp E Scherer · Ut Southwestern Medical Center · RC1 · FY2009 · DK
Markers of the metabolic syndrome linking type 2 diabetes and MI in South Asia
$499,993Daniel James Rader · University Of Pennsylvania · RC1 · FY2009 · TW
Markers of the metabolic syndrome linking type 2 diabetes and MI in South Asia
$499,993Daniel James Rader · University Of Pennsylvania · RC1 · FY2010 · TW
Long-term sequelae of early life pesticide exposure in the CHAMACOS birth cohort
$499,989Brenda Eskenazi · University Of California Berkeley · UH3 · FY2019 · ES
Long-term sequelae of early life pesticide exposure in the CHAMACOS birth cohort
$499,980Brenda Eskenazi · University Of California Berkeley · UH3 · FY2020 · ES
Elucidating mechanisms of SIRT1 activation
$499,967David A. Sinclair · Harvard Medical School · R01 · FY2019 · DK
Translational Systems Genetics of Mitochondria, Metabolism, and Aging
$499,912Robert W. W Williams · University Of Tennessee Health Sci Ctr · R01 · FY2017 · AG