Jose Cordoba-Chacon

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Assistant Professor

University of Chicago

United States

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Jose Cordoba-Chacon is an Assistant Professor at the University of Illinois at Chicago, USA. His research focuses on the molecular mechanisms underlying metabolic diseases, particularly in the context of liver function and pancreatic cancer. His recent publications explore topics such as the role of cell membrane fatty acids in cancer etiology, the implications of hepatic putrescine in metabolic dysfunction, and the influence of gut-derived ammonia on alcohol-related liver disease.

Recent Grants

Grant: Close

Regulation of methionine metabolism in NASH by PPARgamma

Open Date: 2022-06-01

Close Date: 2024-05-01

Grant: Open

PPARgamma-regulated mechanisms in hepatocytes that promote NAFLD

Open Date: 2022-02-01

Close Date: 2027-01-01

Grant: Close

ROLE OF TZD-ACTIVATED PPAR GAMMA IN HEPATOCYTES IN THE DEVELOPMENT AND PROGRESSION OF NASH

Open Date: 2020-01-01

Close Date: 2021-01-01

Grant: Close

Suppression of hepatic glucose production by conjugated linoleic acids

Open Date: 2019-01-01

Close Date: 2021-01-01

Grant: Close

Hepatocyte PPARgamma regulated mechanisms in NAFLD and lipid homeostasis

Open Date: 2018-02-01

Close Date: 2022-12-01

Jose Cordoba-Chacon

Research Interests

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About

Recent Grants

Articles (17)

Modifications of the GH Axis Reveal Unique Sexually Dimorphic Liver Signatures for Lcn13, Asns, Hamp2, Hao2, and Pgc1a

Cell Membrane Fatty Acids and PIPs Modulate the Etiology of Pancreatic Cancer by Regulating AKT.

Increased hepatic putrescine levels as a new potential factor related to the progression of metabolic dysfunction-associated steatotic liver disease.

Intestinal FFA2 promotes obesity by altering food intake in Western diet-fed mice.

Clinical features and immune mechanisms directly linked to the altered liver function in patients with rheumatoid arthritis

Nicotinamide N-methyltransferase upregulation contributes to palmitate-elicited peroxisome proliferator-activated receptor transactivation in hepatocytes

ATF4-mediated CD36 upregulation contributes to palmitate-induced lipotoxicity in hepatocytes

Hepatocyte PPARγ contributes to the progression of non-alcoholic steatohepatitis in male and female obese mice

Role of hepatic peroxisome proliferator-activated receptor γ in non-alcoholic fatty liver disease

Gut-derived ammonia contributes to alcohol-related fatty liver development via facilitating ethanol metabolism and provoking ATF4-dependent de novo lipogenesis activation.

Liver-specific overexpression of HKDC1 increases hepatocyte size and proliferative capacity.

Direct and systemic actions of growth hormone receptor (GHR)-signaling on hepatic glycolysis, de novo lipogenesis and insulin sensitivity, associated with steatosis.

Secreted EMC10 is upregulated in human obesity and its neutralizing antibody prevents diet-induced obesity in mice.

The hexokinase "HKDC1" interaction with the mitochondria is essential for liver cancer progression.

Growth Hormone and Insulin-Like Growth Factor 1 Regulation of Nonalcoholic Fatty Liver Disease

Rosiglitazone Requires Hepatocyte PPARγ Expression to Promote Steatosis in Male Mice With Diet-Induced Obesity

Adipose expression of CREB3L3 modulates body weight during obesity.

Collaborators (7)

Fernando Leiva-Cepas

Rhonda D Kineman

Md. Wasim Khan

CHARY LOPEZ-PEDRERA

Zhenyuan Song

Manuel D. Gahete

Eva Perez-Pampin

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