Effects of Gastric Inhibitory Polypeptide on Glucose and Lipid Metabolism of Isolated Rat Adipocytes

1988 ◽  
Vol 32 (5-6) ◽  
pp. 282-288 ◽  
Author(s):  
H. Hauner ◽  
G. Glatting ◽  
D. Kaminska ◽  
E.F. Pfeiffer
2002 ◽  
Vol 26 (7) ◽  
pp. 912-919 ◽  
Author(s):  
MJ Moreno-Aliaga ◽  
JA Martínez ◽  
KL Stanhope ◽  
MP Fernández-Otero ◽  
PJ Havel

2009 ◽  
Vol 91 (03) ◽  
pp. 350-354 ◽  
Author(s):  
H. Hauner ◽  
G. Glatting ◽  
H. H. Ditschuneit ◽  
E. F. Pfeiffer

1987 ◽  
Vol 15 (01n02) ◽  
pp. 31-42 ◽  
Author(s):  
T.B. Ng ◽  
C.M. Wong ◽  
W.W. Li ◽  
H.W. Yeung

Fruits and seeds of the bitter gourd Momordica charantia (Family Cucurbitaceae) were extracted with the acidic ethanol. The extract was adjusted to pH 3 and proteins and peptides were precipitated by additon of a copious volume of aceton. The precipitate was dissolved, dialyzed and lyophilized. The resulting material, designated "p-fraction" was tested for antilipolytic and lipogenic activities. Seed "p-fraction" was further chromatographed on fetuin agraose to yield an unadsorbed fraction (F) which could be fractioned by gel filtration on Sephadex G-10 to give an unretarted fraction (F1) and a retarted function (F2). Fruit "p-fraction" exhibited antilipolytic activity in hamster adipocytes and stimulated 3H-glucose incorporation into lipids, F1, a saponin containing fraction, inhibited both lipolysis and 3H-glucose incorporation into lipids. F2 enhance 3H-glucose corporation into lipid. The results are indicavie of the presence of compounds with insulinomimetic activities in M. charantia fruits and seeds.


1998 ◽  
Vol 336 (1) ◽  
pp. 163-181 ◽  
Author(s):  
Wendelin FRICK ◽  
Andrea BAUER ◽  
Jochen BAUER ◽  
Susanne WIED ◽  
Günter MÜLLER

A set of synthetic phosphoinositolglycan (PIG) compounds has been demonstrated to exert insulin-mimetic activity on glucose and lipid metabolism in rat adipocytes differing considerably in potency [compound 41 > 37 > 45 ≫ 7 > 1; W. Frick, A. Bauer, J. Bauer, S. Wied and G. Müller, G. (1998) Biochemistry 37, 13421–13436]. In the present study we examine whether these differences are based on the capability of the PIG compounds to stimulate signalling components which are thought to mediate metabolic insulin action. Studies using a tyrosine kinase inhibitor and introduction into adipocytes of anti-phosphotyrosine or inhibitory anti-insulin receptor β-subunit antibodies demonstrated dependence on tyrosine phosphorylation but independence of insulin receptor kinase activation of the insulin-mimetic signalling and metabolic activity of the PIG compounds. The five compounds elicited in rat adipocytes a significant increase in tyrosine phosphorylation of both insulin receptor substrate 1 (IRS-1) and IRS-3 and, to a minor degree, IRS-2, in IRS-1/3-associated phosphatidylinositol 3-kinase (PI 3-K) protein as well as activity, and in protein kinase B (PKB) activity as well as phosphorylation. This was most pronounced for compound 41, approaching 65–95% of the maximal insulin response (MIR) at 20 µM, and declined in the order of compounds 37, 45, 7 and 1. The same ranking was true for the maximal inhibition of glycogen synthase kinase 3 activity (GSK-3) (41, 75% of MIR; compound 37, 65%; compound 7, 25%; compound 1, 10%) and GSK-3 autophosphorylation. The half-maximal concentrations effective for signalling (compound 41, 2–5 µM; compound 37, 10–20 µM) corresponded well to those stimulating glucose and lipid metabolism. Interestingly, compounds 37 and 41 stimulated mitogen-activated protein kinase (MAPK) and protein synthesis in rat adipocytes to only about 20–30% (at 50 µM) of MIR. We conclude that in rat adipocytes: (i) the potency of PIG compounds to regulate glucose/lipid metabolism depends on the activation of PI 3-K and PKB and inhibition of GSK-3; (ii) initiation of tyrosine phosphorylation of IRS-1/3 is sufficient and activation of the PI 3-K cascade is required for insulin-mimetic metabolic signalling; and (iii) PIG compounds are quite selective for the PI 3-K compared to the MAPK cascade, (iv) PIG compounds seem to use the same signalling components downstream of PI 3-K (including Rab4) for stimulation of glucose transport as does insulin. Thus the early signalling step(s) used by PIG, but not by insulin, may represent a target for the treatment of insulin-resistant states.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1060-P
Author(s):  
LIXIN GUO ◽  
QI PAN ◽  
CHAO CHEN ◽  
SHUSHAN LIN ◽  
YU LI ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1878-P
Author(s):  
LIANGHUI YOU ◽  
YU ZENG ◽  
NAN GU ◽  
CHENBO JI

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