Identification of SH2-B as a key regulator of leptin sensitivity, energy balance, and body weight in mice

Cell Metab. 2005 Aug;2(2):95-104. doi: 10.1016/j.cmet.2005.07.004.

Abstract

Leptin regulates energy balance and body weight by activating its receptor LEPRb and multiple downstream signaling pathways, including the STAT3 and the IRS2/PI 3-kinase pathways, in the hypothalamus. Leptin stimulates activation of LEPRb-associated JAK2, which initiates cell signaling. Here we identified SH2-B, a JAK2-interacting protein, as a key regulator of leptin sensitivity, energy balance, and body weight. SH2-B homozygous null mice were severely hyperphagic and obese and developed a metabolic syndrome characterized by hyperleptinemia, hyperinsulinemia, hyperlipidemia, hepatic steatosis, and hyperglycemia. The expression of hypothalamic orexigenic NPY and AgRP was increased in SH2-B(-/-) mice. Leptin-stimulated activation of hypothalamic JAK2 and phosphorylation of hypothalamic STAT3 and IRS2 were significantly impaired in SH2-B(-/-) mice. Moreover, overexpression of SH2-B counteracted PTP1B-mediated inhibition of leptin signaling in cultured cells. Our data suggest that SH2-B is an endogenous enhancer of leptin sensitivity and required for maintaining normal energy metabolism and body weight in mice.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Body Weight*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Enzyme Activation
  • Female
  • Homeostasis*
  • Hypothalamus
  • Insulin Receptor Substrate Proteins
  • Intracellular Signaling Peptides and Proteins
  • Janus Kinase 2
  • Leptin / metabolism*
  • Male
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Obesity / genetics
  • Obesity / metabolism
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • STAT3 Transcription Factor
  • Signal Transduction / physiology
  • Trans-Activators / genetics
  • Trans-Activators / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • DNA-Binding Proteins
  • Insulin Receptor Substrate Proteins
  • Intracellular Signaling Peptides and Proteins
  • Irs2 protein, mouse
  • Leptin
  • Phosphoproteins
  • Proto-Oncogene Proteins
  • STAT3 Transcription Factor
  • Sh2bpsm1 protein, mouse
  • Stat3 protein, mouse
  • Trans-Activators
  • Protein-Tyrosine Kinases
  • Jak2 protein, mouse
  • Janus Kinase 2