Helena C. F. de Oliveira

Principal Investigator
Studies molecular mechanisms linking obesity and insulin resistance to atherosclerosis.
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Institute of Biology – University of Campinas

Lipid Metabolism Laboratory

We focus our investigations on the metabolism of plasmatic lipoproteins and proteins associated with a number of pathophysiological states that are especially relevant to the understanding of atherogenesis and metabolic disorders such as obesity and diabetes. We study the hormonal, nutritional and pharmacological regulation of key proteins in lipoprotein metabolism and seek to clarify the cellular and molecular mechanisms responsible for cardio-metabolic disorders, as well as uncover potential therapeutic targets. The group has made contributions to the understanding of the regulation of cholesteryl ester transfer protein (CETP) expression and its consequences on susceptibility to atherosclerosis, as well as investigated possible new functions for this protein (for review see Oliver & Faria, IUBMB Life , 2011). Along with Professor Anibal Vercesi and his group, we showed that changes in bioenergetic function and mitochondrial redox state are highly relevant cellular and biochemical mechanisms in hyperlipidemia conditions predisposing to atherosclerosis, (Vercesi, IUBMB Life, 2007). Jointly with Professors AC Boschero and Everardo M Carneiro, we demonstrated that genetic hypercholesterolemia impairs the insulin secretory function in pancreatic islets (de Souza et al, Diabetologia, 2010).

TEAM

RESEARCH FELLOW

  • Helena Fonseca Raposo
  • Leandro Henrique de Paula Assis

pHD

  • Carolina Martins Lazaro
  • Thiago Rentz Ferreira

Master

  • Júlia Zago Castelli

main discoveries

  • The CETP (cholesteryl ester transfer protein) gene expression: is upregulated by cholesterol, omega-3 fatty acids and fibrates; is downregulated by insulin but is not regulated by estrogens; depending on the metabolic context, can modulate atherosclerosis; for example, CETP expression attenuates atherosclerosis in sex hormone deficiency and increases plasma cholesterol esterification (increase in LCAT), but does not alter atherosclerosis in diabetes; has a new anti-obesity function;
  • Genetic hyperlipidemias impair mitochondrial function in such a way that increases susceptibility to atherosclerosis and obesity;
  • Primary hypercholesterolemia compromises insulin secretion and raises diabetes risks.

main articles

  • Cholesterol reduction ameliorates glucose-induced calcium handling and insulin secretion in islets from low-density lipoprotein receptor knockout mice
  • Activation of the mitochondrial ATP-sensitive K channel reduces apoptosis of spleen mononuclear cells induced by hyperlipidemia
  • A spontaneous mutation in the nicotinamide nucleotide transhydrogenase gene of C57BL/6J mice results in mitochondrial redox abnormalities
  • Metastasis of Orthotopic Tongue Oral Squamous Cell Carcinomas The Fatty Acid Synthase Inhibitor Orlistat Reduces the Growth and
To contact Helena C. F. de Oliveira's lab use the following information:
Laboratório de Metabolismo de Lípides
Centro de Pesquisa em Obesidade e Comorbidades - 2º Andar
Instituto de Biologia - Bloco Z
Rua Carl Von Linaeus - s/n - Cidade Universitária
Campinas - SP, 13083-864
+55 19 3521-0015