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Acta Physiologica 2009; Volume 197, Supplement 672
The 60th National Congress of the Italian Physiological Society
9/23/2009-9/25/2009
Siena, Italy
INSULIN-MIMETIC ACTION OF CONGLUTIN- IN MOUSE MYOBLASTS
Abstract number: P166
TERRUZZI1 I, SENESI2 P, MONTESANO2 A, MAGNI3 C, SCARAFONI3 A, LUZI1,2 L, DURANTI3 M
1Unit di Nutrizione e Metabolismo, Istituto San Raffaele, Milano
2Dip. Scienze dello Sport, Nutrizione e Salute, Facolt di Scienze Motorie, Univ. degli Studi di Milano
3Dip. di Scienze Molecolari Agroalimentari, Facolt di Agraria, Univ. degli Studi di [email protected]
Aim:
Lupin seed is referred to as an antidiabetic product by the traditional medicine. Conglutin-g, a lupin seed glycoprotein, caused a significant plasma glucose reduction when orally administered upon glucose overload trials in rats. The aim of this work was to unveil conglutin-g hypothetical insulin-mimetic cellular mechanism of action. Insulin is the primary hormone responsible for proteosynthesis control through IRS/P70S6k/PHAS1 pathways modulation, glucose homeostasis and muscle differentiation and hypertrophy via muscle-specific MHC (myosin heavy chain) gene transcription control.
Methods and Results:
To verify if conglutin-g is able to modulate the same insulin-activated kinases, myoblastic C2C12 cells were incubated, after 72h of differentiation, with 100 nM insulin or 0.5 mg/ml conglutin-g. We used cells without stimulation as a negative control and cells stimulated with metformin as a positive control. We evaluated the effect of these treatment after 5, 10, 20, 30 and 240 minutes. We verified that stimulation with insulin or conglutin-g resulted in persistent activation of kinases of the protein synthetic pathway as well as increase of glucose transport and muscle-specific gene transcription regulation.
Conclusion:
Our results indicate that conglutin-g may regulate the same components of the insulin signaling, suggesting the potential therapeutic oral use of this protein in diabetes treatment and, in particular, the potential conglutin-g influence on muscle cells differentiation and hypertrophy.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 197, Supplement 672 :P166