Absence of short-term effects of glucagon-like peptide-1 and of hyperglycemia on plasma leptin levels in man

Metabolism ◽  
1997 ◽  
Vol 46 (7) ◽  
pp. 723-725 ◽  
Author(s):  
Anath Shalev ◽  
Susanna Vosmeer ◽  
Ulrich Keller
2015 ◽  
Vol 308 (4) ◽  
pp. R300-R304 ◽  
Author(s):  
Sina S. Ullrich ◽  
Bärbel Otto ◽  
Amy T. Hutchison ◽  
Natalie D. Luscombe-Marsh ◽  
Michael Horowitz ◽  
...  

Intraduodenal infusion of lipid or protein potently reduces subsequent energy intake. There is evidence that the underlying mechanisms differ significantly between the two nutrients. While intraduodenal lipid stimulates glucagon-like peptide-1 and CCK much more than protein, the release of insulin and glucagon is substantially greater in response to protein. Ghrelin and PYY are both involved in short-term regulation, while leptin is a long-term regulator, of energy balance; the acute effects of nutrients on leptin release are unclear. We investigated the comparative effects of intraduodenal lipid and protein on plasma ghrelin, PYY, and leptin concentrations. Thirteen lean, young men received 90-min intraduodenal infusions of protein (whey hydrolysate) or lipid (long-chain triglyceride emulsion) at a rate of 3 kcal/min, or saline control, on three separate days. Blood samples were collected at baseline and regularly during infusions. Both lipid and protein potently suppressed plasma ghrelin compared with control (both P < 0.001), with no difference between them. While both lipid and protein stimulated plasma PYY ( P < 0.001), the effect of lipid was substantially greater than that of protein ( P < 0.001). Neither intraduodenal lipid nor protein affected plasma leptin. In conclusion, intraduodenal lipid and protein have discrepant effects on the release of PYY, but not ghrelin. When considered with our previous findings, it appears that, with the exception of ghrelin, the energy intake-suppressant effects of lipid and protein are mediated by different mechanisms.


2013 ◽  
Vol 10 (1) ◽  
pp. 33 ◽  
Author(s):  
Danny Wadden ◽  
Farrell Cahill ◽  
Peyvand Amini ◽  
Edward Randell ◽  
Sudesh Vasdev ◽  
...  

1997 ◽  
Vol 34 (3) ◽  
pp. 230-234 ◽  
Author(s):  
C. Drewes ◽  
M. A. Nauck ◽  
R. Horn ◽  
J. Holst ◽  
W. Schmiegel ◽  
...  

2008 ◽  
Vol 178 (2) ◽  
pp. 233-237 ◽  
Author(s):  
Stephanie Van Weyenberg ◽  
Myriam Hesta ◽  
Johan Buyse ◽  
Georgios A. Papadopoulos ◽  
Geert P.J. Janssens

1997 ◽  
Vol 272 (2) ◽  
pp. R726-R730 ◽  
Author(s):  
T. E. Thiele ◽  
G. Van Dijk ◽  
L. A. Campfield ◽  
F. J. Smith ◽  
P. Burn ◽  
...  

Leptin (ob protein) and glucagon-like peptide-1-(7-36) amide (GLP-1) are peptides recently proposed to be involved in the regulation of food intake. Although the ability of exogenous leptin and GLP-1 to modulate consummatory behavior is consistent with the suggestion that these peptides are endogenous regulatory agents, central administration of these peptides may have aversive side effects, which could explain the anorexia. In the present experiment, exposure to a saccharine taste was immediately followed by central administration of leptin or GLP-1 to determine if these drugs could produce a conditioned taste aversion (CTA) in rats. At doses equated for producing comparable reductions in short-term food intake, GLP-1, but not leptin, generated a robust CTA. Although leptin caused no aversion, this peptide was the only drug to cause relatively long-term reductions in food consumption (16 h) and body weight (24 h). Hence, the results indicate that central GLP-1 produces aversive side effects, and it is argued that these nonspecific effects may explain the anorectic actions of GLP-1.


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