Jeffrey M. Zigman

ORCID: 0000-0003-3477-1295
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About
Contact & Profiles
Research Areas
  • Regulation of Appetite and Obesity
  • Biochemical Analysis and Sensing Techniques
  • Adipose Tissue and Metabolism
  • Pancreatic function and diabetes
  • Adipokines, Inflammation, and Metabolic Diseases
  • Sleep and Wakefulness Research
  • Diet and metabolism studies
  • Diet, Metabolism, and Disease
  • Hypothalamic control of reproductive hormones
  • Diabetes and associated disorders
  • Genetic Syndromes and Imprinting
  • Epigenetics and DNA Methylation
  • Neuropeptides and Animal Physiology
  • Eating Disorders and Behaviors
  • Olfactory and Sensory Function Studies
  • Receptor Mechanisms and Signaling
  • Growth Hormone and Insulin-like Growth Factors
  • Plant Reproductive Biology
  • Thyroid Cancer Diagnosis and Treatment
  • Liver Disease Diagnosis and Treatment
  • Nuclear Receptors and Signaling
  • Dietary Effects on Health
  • Apelin-related biomedical research
  • Mast cells and histamine
  • Neuroendocrine Tumor Research Advances

The University of Texas Southwestern Medical Center
2016-2025

Southwestern Medical Center
2010-2024

Southwestern University
2023

The University of Texas at Austin
2012

University of Cincinnati
2007

Beth Israel Deaconess Medical Center
2003-2006

Harvard University
2003-2006

Harvard Vanguard Medical Associates
2003-2004

Hadassah Medical Center
2002

University of Chicago
1993-1994

Ghrelin is a hormone that stimulates growth secretion and signals energy insufficiency via interaction with its receptor, the secretagogue receptor (GHSR). The GHSR located in both central nervous system periphery. Its distribution CNS, as assessed by situ hybridization histochemistry (ISHH), has been described previously few mammalian species, although these studies were limited either detail provided or extent of regions examined. In present study, we systematically examined mRNA adult rat...

10.1002/cne.20823 article EN The Journal of Comparative Neurology 2005-01-01

Ghrelin is the endogenous ligand for growth hormone secretagogue receptor (GHSR; ghrelin receptor). Since its discovery, accumulating evidence has suggested that may play a role in signaling and reversing states of energy insufficiency. For example, levels rise following food deprivation, administration stimulates feeding increases body weight adiposity. However, recent loss-of-function studies have raised questions regarding physiological significance regulating these processes. Here, we...

10.1172/jci26002 article EN Journal of Clinical Investigation 2005-12-01

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

The popular media and personal anecdotes are rich with examples of stress-induced eating calorically dense "comfort foods." Such behavioral reactions likely contribute to the increased prevalence obesity in humans experiencing chronic stress or atypical depression. However, molecular substrates neurocircuits controlling complex behaviors responsible for stress-based remain mostly unknown, few animal models have been described probing mechanisms orchestrating this response. Here, we describe...

10.1172/jci57660 article EN Journal of Clinical Investigation 2011-06-23

Drugs activating 5-hydroxytryptamine 2C receptors (5-HT2CRs) potently suppress appetite, but the underlying mechanisms for these effects are not fully understood. To tackle this issue, we generated mice with global 5-HT2CR deficiency (2C null) and 5-HT2CRs re-expression only in pro-opiomelanocortin (POMC) neurons (2C/POMC mice). We show that null predictably developed hyperphagia, hyperactivity, obesity showed attenuated responses to anorexigenic 5-HT drugs. Remarkably, all deficiencies were...

10.1016/j.neuron.2008.09.033 article EN cc-by Neuron 2008-11-01

Enteroendocrine cells such as duodenal cholecystokinin (CCK cells) are generally thought to be confined certain segments of the gastrointestinal (GI) tract and store release peptides derived from only a single peptide precursor. In current study, however, transgenic mice expressing enhanced green fluorescent protein (eGFP) under control CCK promoter demonstrated distribution pattern CCK-eGFP positive that extended throughout intestine. Quantitative PCR liquid chromatography-mass spectrometry...

10.1210/en.2012-1595 article EN Endocrinology 2012-10-13

The molecular mechanisms regulating secretion of the orexigenic-glucoregulatory hormone ghrelin remain unclear. Based on qPCR analysis FACS-purified gastric cells, highly expressed and enriched 7TM receptors were comprehensively identified functionally characterized using in vitro, ex vivo methods. Five Gαs-coupled efficiently stimulated secretion: as expected β1-adrenergic, GIP secretin but surprisingly also composite receptor for sensory neuropeptide CGRP melanocortin 4 receptor. A number...

10.1016/j.molmet.2013.08.006 article EN cc-by-nc-sa Molecular Metabolism 2013-09-04

Ghrelin targets the hypothalamus to regulate food intake and adiposity. Endogenous ghrelin receptors [growth hormone secretagogue receptor (GHSR)] are also present in extrahypothalamic sites where they promote circuit activity associated with learning memory, reward seeking behavior. Here, we show that substantia nigra pars compacta (SNpc), a brain region dopamine (DA) cell degeneration leads Parkinson's disease (PD), expresses GHSR. binds SNpc cells, electrically activates DA neurons,...

10.1523/jneurosci.3890-09.2009 article EN cc-by-nc-sa Journal of Neuroscience 2009-11-11

The hormone ghrelin stimulates eating and helps maintain blood glucose upon caloric restriction. While previous studies have demonstrated that hypothalamic arcuate AgRP neurons are targets of ghrelin, the overall relevance signaling within intact is unclear. Here, we tested functional significance action on using a new, tamoxifen-inducible AgRP-CreER(T2) transgenic mouse model allows spatiotemporally-controlled re-expression physiological levels receptors (GHSRs) specifically in adult...

10.1016/j.molmet.2013.10.001 article EN cc-by-nc-sa Molecular Metabolism 2013-10-17

Acyl-ghrelin administration increases food intake, body weight, and blood glucose. In contrast, mice lacking ghrelin or receptors (GHSRs) exhibit life-threatening hypoglycemia during starvation-like conditions, but do not consistently overt metabolic phenotypes when given ad libitum access. These results, findings of resistance in obese states, imply nutritional state dependence ghrelin's actions. Here, we hypothesized that liver-enriched antimicrobial peptide-2 (LEAP2), a recently...

10.1172/jci125332 article EN Journal of Clinical Investigation 2019-08-18

Ghrelin, the only known orexigenic gut hormone, is secreted mainly from stomach, increases with fasting and before meal initiation in humans rats, food intake after central or peripheral administration. To investigate sex differences action of ghrelin, we assessed effects exogenous ghrelin intact male female ovariectomized (OVX) estradiol (E2)-treated as well OVX on plasma hypothalamic orexigneic neuropeptide expression rats weight gain transgenic mice lacking receptor (Ghsr−/− mice). Male...

10.2337/db06-0015 article EN Diabetes 2007-03-29

Ghrelin, an octanoylated peptide hormone produced in the stomach, rises dramatically mouse plasma during chronic severe calorie deprivation, event that is essential to maintain life. The mechanism for this increase not understood. Here, we study control of ghrelin secretion tissue culture cells derived from mice bearing ghrelinomas induced by a tissue-specific SV40 T-antigen transgene. We found ghrelin-secreting express high levels mRNA encoding β 1 -adrenergic receptors. Addition...

10.1073/pnas.1011116107 article EN Proceedings of the National Academy of Sciences 2010-08-16

ABSTRACT Growth hormone secretagogue receptor (GHSR) 1a is the only molecularly identified for ghrelin, mediating ghrelin‐related effects on eating, body weight, and blood glucose control, among others. The expression pattern of GHSR within brain has been assessed previously by several neuroanatomical techniques. However, inherent limitations to these techniques lack reliable anti‐GHSR antibodies reporter rodent models that identify GHSR‐containing neurons have prevented a more comprehensive...

10.1002/cne.23627 article EN The Journal of Comparative Neurology 2014-05-14

Circulating ghrelin elevates abdominal adiposity by a mechanism independent of its central orexigenic activity. In this study we tested the hypothesis that peripheral induces depot-specific increase in white adipose tissue (WAT) mass vivo GH secretagogue receptor (GHS-R(1a))-mediated lipolysis. Chronic iv infusion acylated increased retroperitoneal and inguinal WAT volume rats without elevating superficial sc fat, food intake, or circulating lipids glucose. Increased resulted from adipocyte...

10.1210/me.2008-0432 article EN Molecular Endocrinology 2009-03-20
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