The aim of the present study was to evaluate the effect of a chronic oral gamma-conglutin treatment in male Sprague – Dawley rats in which hyperglycaemia had been induced by supplying 10 % D-glucose in drinking-water. A gamma-conglutin dosage of 28 mg/kg body weight was daily administered to animals for 21 d. Plasma glucose, insulin and glucose overloading were monitored. Chronic administration of glucose resulted in a statistically significant (P< 0·05) increase in fasting blood glucose (2·5-fold) and insulin (2·7-fold) v. the values recorded in control rats. Simultaneous treatment with gamma-conglutin attenuated the rise in plasma glucose (1·9-fold) and insulin (1·8-fold) levels in the glucose-fed rats (P< 0·05). Fasting insulin and homeostasis model of insulin resistance were decreased by 34 and 48 % (P< 0·05), respectively, in the gamma-conglutin-treated rats v. the values found in pair-fed animals. To confirm these results with a different approach, HepG2 cells, grown for 24 and 48 h in Dulbecco’s minimum essential medium containing different glucose concentrations (5·5, 11·1 and 16·5 mmol/l), were exposed to 10 mmol/l gamma-conglutin with or without 10 mmol/l metformin or 100 nmol/l insulin. Gamma-conglutin increased glucose consumption (from 1·5- to 2·5-fold) in HepG2 cells, under all experimental conditions; this effect was more evident after 48 h incubation. Moreover, in this in vitro model, the addition of gamma-conglutin potentiated the activity of insulin and metformin in cell glucose consumption. These findings extend the previous ones and suggest the potential use of lupin gamma-conglutin in the control of glycaemia.

Lupin seed γ-conglutin lowers blood glucose in hyperglycaemic rats and increases glucose consumption of HepG2 cells / M.R. Lovati, C. Manzoni, S. Castiglioni, A. Parolari, C. Magni, M. Duranti. - In: BRITISH JOURNAL OF NUTRITION. - ISSN 0007-1145. - 107:1(2012 Jan 14), pp. 67-73. [10.1017/S0007114511002601]

Lupin seed γ-conglutin lowers blood glucose in hyperglycaemic rats and increases glucose consumption of HepG2 cells

M.R. Lovati;C. Manzoni;S. Castiglioni;C. Magni;M. Duranti
2012

Abstract

The aim of the present study was to evaluate the effect of a chronic oral gamma-conglutin treatment in male Sprague – Dawley rats in which hyperglycaemia had been induced by supplying 10 % D-glucose in drinking-water. A gamma-conglutin dosage of 28 mg/kg body weight was daily administered to animals for 21 d. Plasma glucose, insulin and glucose overloading were monitored. Chronic administration of glucose resulted in a statistically significant (P< 0·05) increase in fasting blood glucose (2·5-fold) and insulin (2·7-fold) v. the values recorded in control rats. Simultaneous treatment with gamma-conglutin attenuated the rise in plasma glucose (1·9-fold) and insulin (1·8-fold) levels in the glucose-fed rats (P< 0·05). Fasting insulin and homeostasis model of insulin resistance were decreased by 34 and 48 % (P< 0·05), respectively, in the gamma-conglutin-treated rats v. the values found in pair-fed animals. To confirm these results with a different approach, HepG2 cells, grown for 24 and 48 h in Dulbecco’s minimum essential medium containing different glucose concentrations (5·5, 11·1 and 16·5 mmol/l), were exposed to 10 mmol/l gamma-conglutin with or without 10 mmol/l metformin or 100 nmol/l insulin. Gamma-conglutin increased glucose consumption (from 1·5- to 2·5-fold) in HepG2 cells, under all experimental conditions; this effect was more evident after 48 h incubation. Moreover, in this in vitro model, the addition of gamma-conglutin potentiated the activity of insulin and metformin in cell glucose consumption. These findings extend the previous ones and suggest the potential use of lupin gamma-conglutin in the control of glycaemia.
hyperglycaemic rats ; lupinus albus seed protein ; gamma-conglutin ; hepG2 cells ; glucose consumption
Settore BIO/14 - Farmacologia
Settore BIO/10 - Biochimica
14-gen-2012
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/161348
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