João Paulo Camporez

ORCID: 0000-0003-3486-4301
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About
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Research Areas
  • Adipose Tissue and Metabolism
  • Pancreatic function and diabetes
  • Liver Disease Diagnosis and Treatment
  • Metabolism, Diabetes, and Cancer
  • Diet, Metabolism, and Disease
  • Growth Hormone and Insulin-like Growth Factors
  • Lipid metabolism and disorders
  • Adipokines, Inflammation, and Metabolic Diseases
  • Diet and metabolism studies
  • Lipid metabolism and biosynthesis
  • Hormonal and reproductive studies
  • Regulation of Appetite and Obesity
  • Mitochondrial Function and Pathology
  • Peroxisome Proliferator-Activated Receptors
  • Hormonal Regulation and Hypertension
  • Ovarian function and disorders
  • Fibroblast Growth Factor Research
  • Diabetes and associated disorders
  • Muscle metabolism and nutrition
  • Kruppel-like factors research
  • Cancer, Hypoxia, and Metabolism
  • Epigenetics and DNA Methylation
  • Endoplasmic Reticulum Stress and Disease
  • Sirtuins and Resveratrol in Medicine
  • Autophagy in Disease and Therapy

Universidade de São Paulo
2011-2025

Yale University
2014-2024

Universidade de Ribeirão Preto
2021

University of New Haven
2016-2018

Inova Fairfax Hospital
2017

Yale Cancer Center
2012-2014

Cambridge University Press
2013

New York University Press
2013

Howard Hughes Medical Institute
2011

Institute of Biomedical Science
2008-2010

Significance Chronic low-grade inflammation is a key driver of metabolic syndrome. This inflammatory response mediated by immune-cell infiltration and the expression cytokines. IL6 implicated in this response, but physiological role signaling unclear. Here, we demonstrate that source influences nature response. We report secreted myeloid cells inhibits adipose tissue macrophage (ATM) accumulation canonical mechanism, adipocytes or muscle promotes ATM noncanonical mechanism. These...

10.1073/pnas.1920004117 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2020-01-24

Fibroblast growth factor 21 (FGF21) is a potent regulator of glucose and lipid metabolism currently being pursued as therapeutic agent for insulin resistance type 2 diabetes. However, the cellular mechanisms by which FGF21 modifies action in vivo are unclear. To address this question, we assessed regular chow– high-fat diet (HFD)–fed wild-type mice chronically infused with or vehicle. Here, show that administration results improvements both hepatic peripheral sensitivity HFD-fed mice. This...

10.1210/en.2013-1191 article EN Endocrinology 2013-06-13

Significance The paradox of selective hepatic insulin resistance, wherein the insulin-resistant liver fails to suppress glucose production but continues produce triglycerides, is central pathophysiology type 2 diabetes. We hypothesized that triglyceride synthesis regulated mostly by fatty acid delivery and independent changes in signaling. To examine this hypothesis, we used a novel LC-MS/MS method measure rates esterification vivo. In contrast de novo lipogenesis, acids into was primarily...

10.1073/pnas.1423952112 article EN Proceedings of the National Academy of Sciences 2015-01-06

Zipping up obesity Chylomicrons are specialized particles that carry dietary fats from the intestine to bloodstream for absorption into body. Lacteals lymphatic vessels act as highway chylomicron transport, but it is unclear how passage occurs. Zhang et al. report two endothelial cell receptors, neuropilin-1 (NRP1) and vascular growth factor receptor 1 (VEGFR1, also known FLT1), required convert entry spaces between lacteals open junctions closed, zipped structures (see Perspective by...

10.1126/science.aap9331 article EN Science 2018-08-10

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with cardiometabolic risk. Although studies have shown that estradiol positively contributes to energy metabolism via estrogen receptor alpha (ERα), its role specifically in the not defined. Therefore, this study aimed evaluate effects of ERα overexpression, mice fed a high-fat diet (HFD). Methods: Male C57BL/6J were divided into four groups, vehicle regular chow (RC) (RC-Vehicle); an HFD...

10.3390/pathophysiology32010001 article EN cc-by Pathophysiology 2025-01-03

Estrogen replacement therapy reduces the incidence of type 2 diabetes in postmenopausal women; however, mechanism is unknown. Therefore, aim this study was to evaluate metabolic effects estrogen an experimental model menopause. At 8 weeks age, female mice were ovariectomized (OVX) or sham (SHAM) operated, and OVX treated with vehicle estradiol (E2) (OVX+E2). After 4 high-fat diet feeding, had increased body weight fat mass compared SHAM OVX+E2 mice. displayed reduced whole-body energy...

10.1210/en.2012-1989 article EN Endocrinology 2013-01-31

Significance Sarcopenia, or aging-associated muscle atrophy, increases the risk of falls and fractures is associated with metabolic disease. Because skeletal a major contributor to glucose handling after meal, sarcopenia has significant effects on whole-body metabolism. Despite high prevalence potentially devastating consequences sarcopenia, no effective therapies are available. Here, we show that treatment mice an anti-myostatin antibody for just 4 wk increased mass strength in both young...

10.1073/pnas.1525795113 article EN Proceedings of the National Academy of Sciences 2016-02-08

Comparative gene identification 58 (CGI-58) is a lipid droplet-associated protein that promotes the hydrolysis of triglyceride by activating adipose lipase. Loss-of-function mutations in CGI-58 humans lead to Chanarin–Dorfman syndrome, condition which accumulates various tissues, including skin, liver, muscle, and intestines. Therefore, without adequate expression, lipids are stored rather than used for fuel, signaling intermediates, membrane biosynthesis. knockdown mice using antisense...

10.1073/pnas.1219456110 article EN Proceedings of the National Academy of Sciences 2013-01-09

Lower adipose-ChREBP and de novo lipogenesis (DNL) are associated with insulin resistance in humans. Here, we generated adipose-specific ChREBP knockout (AdChREBP KO) mice negligible sucrose-induced DNL adipose tissue (AT). Chow-fed AdChREBP KO resistant impaired action the liver, muscle, AT increased inflammation. HFD-fed also more than controls. Surprisingly, adipocytes lacking display a cell-autonomous reduction insulin-stimulated glucose transport that is mediated by Glut4 translocation...

10.1016/j.celrep.2017.09.091 article EN cc-by-nc-nd Cell Reports 2017-10-01

Alterations in ectopic lipid deposition and circulating lipids are major risk factors for developing cardiometabolic diseases. Angiopoietin-like protein 4 (ANGPTL4), a that inhibits lipoprotein lipase (LPL), controls fatty acid (FA) uptake adipose oxidative tissues regulates triacylglycerol-rich (TAG-rich) lipoproteins. Unfortunately, global depletion of ANGPTL4 results severe metabolic abnormalities, inflammation, fibrosis when mice fed high-fat diet (HFD), limiting our understanding the...

10.1172/jci.insight.97918 article EN JCI Insight 2018-03-21

Aging is associated with visceral adiposity, metabolic disorders, and chronic low-grade inflammation. 17α-estradiol (17α-E2), a naturally occurring enantiomer of 17β-estradiol (17β-E2), extends life span in male mice through unresolved mechanisms. We tested whether 17α-E2 could alleviate age-related dysfunction reduced body mass, ectopic lipid deposition without decreasing lean mass. These declines were reductions energy intake due to the activation hypothalamic anorexigenic pathways direct...

10.1093/gerona/glv309 article EN cc-by-nc The Journals of Gerontology Series A 2016-01-24

While therapeutic modulation of miRNAs provides a promising approach for numerous diseases, the promiscuous nature raises concern over detrimental off-target effects. miR-33 has emerged as likely target treatment cardiovascular diseases. However, deleterious effects long-term anti-miR-33 therapies and predisposition miR-33−/− mice to obesity metabolic dysfunction exemplify possible pitfalls miRNA-based therapies. Our work an in-depth characterization explores mechanisms by which loss...

10.1016/j.celrep.2018.01.074 article EN cc-by-nc-nd Cell Reports 2018-02-01
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