Streamson C. Chua

ORCID: 0000-0002-9437-9925
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About
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Research Areas
  • Regulation of Appetite and Obesity
  • Adipose Tissue and Metabolism
  • Biochemical Analysis and Sensing Techniques
  • Adipokines, Inflammation, and Metabolic Diseases
  • Pancreatic function and diabetes
  • Hypothalamic control of reproductive hormones
  • Neuropeptides and Animal Physiology
  • Lipid metabolism and biosynthesis
  • Circadian rhythm and melatonin
  • Diet, Metabolism, and Disease
  • Metabolism, Diabetes, and Cancer
  • Genetic Mapping and Diversity in Plants and Animals
  • Calcium signaling and nucleotide metabolism
  • Ovarian function and disorders
  • Trypanosoma species research and implications
  • Diet and metabolism studies
  • Growth Hormone and Insulin-like Growth Factors
  • Sleep and Wakefulness Research
  • FOXO transcription factor regulation
  • Renal Diseases and Glomerulopathies
  • RNA Research and Splicing
  • RNA modifications and cancer
  • Fibroblast Growth Factor Research
  • Cancer, Lipids, and Metabolism
  • Endoplasmic Reticulum Stress and Disease

Albert Einstein College of Medicine
2015-2025

Yeshiva University
2005-2015

Toronto Western Hospital
2012

The University of Texas Southwestern Medical Center
2007-2012

Brigham and Women's Hospital
2012

Harvard University
2012

University of British Columbia
2008

National Cancer Institute
2007

Division of Cancer Epidemiology and Genetics
2007

University of Washington
2007

Mice harboring mutations in the obese ( ob ) and diabetes db genes display similar phenotypes, it has been proposed that these encode ligand receptor, respectively, for a physiologic pathway regulates body weight. The cloning of , demonstration encodes secreted protein (leptin) binds specifically to receptor (OB-R) brain, have validated critical aspects this hypothesis. Here is shown by genetic mapping genomic analysis mouse rat fatty (a homolog ), gene encoding OB-R are same gene.

10.1126/science.271.5251.994 article EN Science 1996-02-16

Adipocytes are embedded in a unique extracellular matrix whose main function is to provide mechanical support, addition participating variety of signaling events. During adipose tissue expansion, the requires remodeling accommodate adipocyte growth. Here, we demonstrate general upregulation several components diabetic state, therefore implicating "adipose fibrosis" as hallmark metabolically challenged adipocytes. Collagen VI highly enriched component tissue. The absence collagen results...

10.1128/mcb.01300-08 article EN Molecular and Cellular Biology 2008-12-30

We have generated mice that carry a neuron-specific leptin receptor (LEPR) transgene whose expression is driven by the rat synapsin I promoter synapsin-LEPR B (SYN-LEPR-B). also are compound hemizygotes for transgenes SYN-LEPR-B and enolase-LEPR (NSE-LEPR-B). observed degree of correction in db/db hemizygous (Syn db/db) homozygous (Syn/Syn similar to previously reported NSE-LEPR-B transgene. show complete obesity related phenotypes both (Nse+Syn db/db). Body composition, insulin sensitivity,...

10.1172/jci24059 article EN Journal of Clinical Investigation 2005-11-11

Studies in humans and rodents indicate that a minimum amount of stored energy is required for normal pubertal development. The adipocyte-derived hormone leptin key metabolic signal to the neuroendocrine reproductive axis. Humans mice lacking or receptor (LepR) (ob/ob db/db mice, respectively) are infertile fail enter puberty. Leptin administration leptin-deficient subjects ob/ob induces puberty restores fertility, but exact site sites action unclear. Here, we found genetic deletion LepR...

10.1172/jci45106 article EN Journal of Clinical Investigation 2010-12-23

Two known types of leptin-responsive neurons reside within the arcuate nucleus: agouti gene-related peptide (AgRP)/neuropeptide Y (NPY) neuron and proopiomelanocortin (POMC) neuron. By deleting leptin receptor gene (Lepr) specifically in AgRP/NPY and/or POMC mice, we examined several combined contributions these to action. Body weight adiposity were increased by Lepr deletion from AgRP individually, simultaneous both (A+P LEPR-KO mice) further measures. Young (periweaning) A+P mice exhibit...

10.1210/en.2007-1132 article EN Endocrinology 2007-12-27

Hepatic steatosis is often associated with insulin resistance and obesity can lead to steatohepatitis cirrhosis. In this study, we have demonstrated that hormone-sensitive lipase (HSL) adipose triglyceride (ATGL), two enzymes critical for lipolysis in tissues, also contribute the liver mobilize hepatic triglycerides vivo vitro. Adenoviral overexpression of HSL and/or ATGL reduced by 40-60% both ob/ob mice high fat diet-induced obesity. However, these did not affect fasting plasma free fatty...

10.1074/jbc.m800533200 article EN cc-by Journal of Biological Chemistry 2008-03-13

Background: In a previous study of Chinese men, we found that men with higher waist-to-hip ratio (WHR) have prostate cancer risk. Because leptin and insulin are related to body fat distribution, examined whether were associated Methods: Blood samples collected from 128 case patients incident 306 healthy control subjects randomly selected residents Shanghai, China. Epidemiologic information anthropometric measurements in personal interviews. Serum leptin, insulin, sex hormone levels measured...

10.1093/jnci/93.10.783 article EN JNCI Journal of the National Cancer Institute 2001-05-16

The rat fatty (fa) mutation produces profound obesity of early onset caused by hyperphagia, defective nonshivering thermogenesis, and preferential deposition energy into adipose tissue. Genetic mapping studies indicate that fa diabetes (db) are homologous loci in the mouse genomes, respectively. It has been shown db alleles carry mutations Lepr (leptin receptor) gene. This paper describes a point allele Lepr. A nucleotide substitution at position 880 (A-->C) causes an amino acid 269...

10.2337/diab.45.8.1141 article EN Diabetes 1996-08-01

Diabetic kidney disease has been associated with the presence of lipid deposits, but mechanisms for accumulation have not fully determined. In present study, we found that db/db mice on FVB genetic background loss-of-function mutation leptin receptor (FVB-Leprdb or FVBdb/db) develop severe diabetic nephropathy, including glomerulosclerosis, tubulointerstitial fibrosis, increased expression type IV collagen and fibronectin, proteinuria, which is renal mRNA abundance transforming growth...

10.2337/diabetes.54.8.2328 article EN Diabetes 2005-08-01

The osteoblast-secreted molecule osteocalcin favors insulin secretion, but how this function is regulated in vivo by extracellular signals for now unknown. In study, we show that leptin, which instead inhibits partly uses the sympathetic nervous system to fulfill function. Remarkably, our purpose, an osteoblast-specific ablation of signaling results a leptin-dependent hyperinsulinemia. osteoblasts, tone stimulates expression Esp, gene inhibiting activity osteocalcin, secretagogue....

10.1083/jcb.200809113 article EN cc-by-nc-sa The Journal of Cell Biology 2008-12-22

The recently identified mouse obese (ob) gene apparently encodes a secreted protein that may function in the signaling pathway of adipose tissue. Mutations ob are associated with early development gross obesity. A detailed knowledge concerning RNA expression pattern and precise genomic location human homolog, OB gene, would facilitate examination role this inheritance Northern blot analysis revealed is present at high level tissue but much lower levels placenta heart. undetectable wide range...

10.1101/gr.5.1.5 article EN Genome Research 1995-08-01

Because high waist-to-hip ratio (WHR) and serum insulin levels have been reported to be associated with an increased risk of prostate cancer, we assessed the relationship between resistance cancer in Chinese men. We measured fasting glucose 128 case 306 control subjects used homeostasis model assessment derive indices sensitivity resistance. Relative men lowest tertiles, highest tertile had a reduced (odds [OR] = 0.35, 95% confidence interval [CI] 0.21 0.60), but (OR 2.78, CI 1.63 4.72)....

10.1093/jnci/95.1.67 article EN JNCI Journal of the National Cancer Institute 2002-12-31
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