Licio Augusto Velloso

Estuda mecanismos moleculares e celulares que levam à disfunção hipotalâmica na obesidade. Palavras-chave: obesidade, hipotálamo, inflamação.

School of Medical Sciences – University of Campinas Laboratory of Cell Signaling The main objective of our group is to identify potential targets for the treatment of obesity. Most recent efforts are focused on the characterization of the cellular and molecular mechanisms involved in the abnormal control of food intake and energy expenditure by the hypothalamus. In 2005, we published the first evidence for a role of diet-induced hypothalamic inflammation as a determining event leading to a dysfunction of the hypothalamus in obesity. In 2009, we showed that TLR4 and endoplasmic reticulum stress are activated in the hypothalamus by dietary fats. Also, we were the first to report the increased rate of neuronal apoptosis in the hypothalamus of obese rodents. In 2011 we used functional magnetic resonance to provide the first evidence for a dysfunction of the hypothalamus of obese subjects. Currently, the lab is working in both human and animal studies searching for novel potential candidates for the development of therapeutic approaches for obesity.


Technical staff

  • Erika Anne de Freitas Robles Roman
  • Gerson Júlio Nery Ferraz
  • Joseane Morari


  • Ana Carolina Marques
  • Carina Solon da Silva
  • Daiane Fátima Engel
  • Guilherme Augusto da Silva Nogueira
  • Milena Monfort Pires
  • Thiago Matos Ferreira de Araújo


  • Alexandre Moura Assis
  • Davi Sidarta Vitória Rodrigues de Oliveira
  • Letícia da Silva Pires
  • Pedro Augusto Silva Nogueira
  • Rodrigo Scarpari Carraro
  • Rodrigo Stellzer Gaspar


  • Ariane Maria Zanesco
  • Marcela Reymond Simões


  • Caio Fernando Biolcatti


  • Researchers at the Cell Signaling Laboratory demonstrated that the intake of diets rich in saturated fats promote damage to the hypothalamus – the brain region that controls hunger. Such damages are due to the activation of an inflammatory response. The persistence of this inflammation can lead to the death of neurons, making treatment even more difficult for this disease;
  • The Cell Signaling Laboratory developed methods to study the function of the hypothalamus in human patients, which has helped create parallels between the disease in experimental models and in humans.


  • TNF-α Mediates PKR-Dependent Memory Impairment and Brain IRS-1 Inhibition Induced by Alzheimer’s β-Amyloid Oligomers in Mice and Monkeys
  • Melatonin acts through MT1/MT2 receptors to activate hypothalamic Akt and suppress hepatic gluconeogenesis in rats
  • Hypothalamic AMPK activation blocks lipopolysaccharide inhibition of glucose production in mice liver
  • Type 2 diabetes mellitus—an autoimmunedisease?
  • Hypothalamic Inhibition of Acetyl-CoA Carboxylase Stimulates Hepatic Counter-Regulatory Response Independent of AMPK Activation in Rats
  • Defective regulation of adipose tissue autophagy in obesity
  • Corticosteroid effect upon intestinal and hepatic interleukin profile in a gastroschisis rat model¹
  • Toll-like receptor 4, F4/80 and pro-inflammatory cytokines in intestinal and mesenteric fat tissue of Crohn’s disease
  • Inhibition of 72 kDa inositol polyphosphate 5-phosphatase E improves insulin signal transduction in diet-induced obesity
  • In?iximab prevents increased systolic blood pressure and upregulates the AKT/eNOS pathway in the aorta of spontaneously hypertensive rats
  • Targeted Disruption of Inducible Nitric Oxide Synthase Protects Against Aging, S-Nitrosation, and Insulin Resistance in Muscle of Male Mice
  • Tub Has a Key Role in Insulin and Leptin Signaling and Action In Vivo in Hypothalamic Nuclei
  • Cerebrospinal ?uid xenin levels during body mass reduction: no evidence for obesity-associated defective transport across the blood—brain barrier
Para entrar em contato com Licio Augusto Velloso e seu laboratório utilize as informações a seguir:
Laboratório de Sinalização Celular
Centro de Pesquisa em Obesidade e Comorbidades - 1º Andar
Instituto de Biologia - Bloco Z
Rua Carl Von Linaeus - s/n - Cidade Universitária
Campinas - SP, 13083-864
+55 19 3521-0026 ou 3521-0025