scholarly journals South American herbal extracts reduce food intake through modulation of gastrointestinal hormones in overweight and obese women

2017 ◽  
Vol 35 ◽  
pp. 555-563 ◽  
Author(s):  
Marina Monteiro Celestino ◽  
Aline Corado Gomes ◽  
Patrícia Borges Botelho ◽  
Alessandra Gambero ◽  
Leonardo Mendes Mesquita ◽  
...  
2010 ◽  
Vol 298 (4) ◽  
pp. R1061-R1067 ◽  
Author(s):  
Thomas Riediger ◽  
Nicole Eisele ◽  
Caroline Scheel ◽  
Thomas A. Lutz

Glucagon-like peptide 1 (GLP-1) and oxyntomodulin (OXM) are structurally related gastrointestinal hormones that are secreted in response to food intake. They reduce food intake and body weight and exert partly overlapping actions on glucose homeostasis and gastrointestinal function. The hypothalamic arcuate (ARC) nucleus is among the central structures expressing a high density of GLP-1 receptors (GLP-1R), which are known to be activated by both peptides. It was the aim of our electrophysiological studies to characterize the effects of GLP-1 and OXM on functionally defined ghrelin-sensitive ARC neurons. GLP-1 and OXM (10−7 M) exerted excitatory effects in about two-thirds of ghrelin-inhibited neurons and in approximately one-third of ghrelin-excited cells. In addition, a minor fraction of the ghrelin-excited cells was inhibited by both peptides. There was a high degree of cosensitivity to GLP-1 and OXM, and the effects of both hormones were blocked by the GLP-1R antagonist exendin(9–39). The GLP-1R-mediated excitations and inhibitions persisted under synaptic blockade, indicating a direct postsynaptic mode of action. Our results demonstrate that GLP-1 and OXM directly and similarly alter neuronal activity in the ARC, probably via a common GLP-1R-mediated mechanism. Ghrelin-antagonistic effects on neuronal activity, which might be implicated in ghrelin-antagonistic in vivo actions, resulting from GLP-1R stimulation (e.g., GLP-1R dependent supression of food intake), predominated in ghrelin-inhibited ARC neurons. However, a subset of ghrelin-excited ARC neurons showed responses to OXM or GLP-1, suggesting the existence of a common mode of action for these hormones; the functional relevance of this effect remains to be elucidated.


Peptides ◽  
1987 ◽  
Vol 8 (3) ◽  
pp. 455-459 ◽  
Author(s):  
Francesco Cavagnini ◽  
Amneris Magella ◽  
Leila Danesi ◽  
Chiara De Paolis ◽  
Rosaria Farina ◽  
...  

2014 ◽  
Vol 144 (12) ◽  
pp. 2018-2026 ◽  
Author(s):  
Ruth W Kimokoti ◽  
Suzanne E Judd ◽  
James M Shikany ◽  
PK Newby

2012 ◽  
Vol 303 (8) ◽  
pp. R850-R860 ◽  
Author(s):  
Miriam Goebel-Stengel ◽  
Andreas Stengel ◽  
Lixin Wang ◽  
Gordon Ohning ◽  
Yvette Taché ◽  
...  

Various molecular forms of CCK reduce food intake in rats. Although CCK-8 is the most studied form, we reported that CCK-58 is the only detectable endocrine peptide form in rats. We investigated the dark-phase rat chow intake pattern following injection of CCK-8 and CCK-58. Ad libitum-fed male Sprague-Dawley rats were intraperitoneally injected with CCK-8, CCK-58 (0.6, 1.8, and 5.2 nmol/kg), or vehicle. Food intake pattern was assessed during the dark phase using an automated weighing system that allowed continuous undisturbed monitoring of physiological eating behavior. Both CCK-8 and CCK-58 dose dependently reduced 1-h, dark-phase food intake, with an equimolar dose of 1.8 nmol being similarly effective (−49% and −44%). CCK-58 increased the latency to the first meal, whereas CCK-8 did not. The intermeal interval was reduced after CCK-8 (1.8 nmol/kg, −41%) but not after CCK-58. At this dose, CCK-8 increased the satiety ratio by 80% and CCK-58 by 160%, respectively, compared with vehicle. When behavior was assessed manually, CCK-8 reduced locomotor activity (−31%), whereas grooming behavior was increased (+59%). CCK-58 affected neither grooming nor locomotor activity. In conclusion, reduction of food intake by CCK-8 and CCK-58 is achieved by differential modulation of food intake microstructure and behavior. These data highlight the importance of studying the molecular forms of peptides that exist in vivo in tissue and circulation of the animal being studied.


1995 ◽  
Vol 89 (4) ◽  
pp. 375-381 ◽  
Author(s):  
Anne Ballinger ◽  
Lorraine McLoughlin ◽  
Sami Medbak ◽  
Michael Clark

1. Intravenous infusions of the brain/gut hormone, cholecystokinin, have been shown to reduce food intake in a subsequent test meal. However, in previous studies the doses administered were large and likely to have produced plasma concentrations far in excess of the normal post-prandial range. 2. In this study cholecystokinin-8 was infused intravenously to six healthy subjects in doses that reproduced physiological post-prandial concentrations. Plasma concentrations of cholecystokinin were measured using a novel sensitive and specific radioimmunoassay. The effect of cholecystokinin-8 infusion on subsequent food intake in a standard test meal was compared with the effect of saline infusion in the same subjects. 3. Food intake (mean ± SEM) was significantly less during cholecystokinin (5092 ± 665 kJ) than during saline infusion (6418 ± 723 kJ, P = 0.03). During cholecystokinin infusion, plasma concentrations increased from 0.45 ± 0.06 pmol/l to 7.28 ± 2.43 pmol/l immediately before the meal. With saline infusion there was no premeal increase in plasma cholecystokinin concentration. 4. This paper describes a novel radioimmunoassay for measurement of plasma concentrations of cholecystokinin. Using this assay we have demonstrated that cholecystokinin is important in control of satiety in humans.


2004 ◽  
Vol 36 (11/12) ◽  
pp. 846-851 ◽  
Author(s):  
W. S. Dhillo ◽  
S. R. Bloom

1996 ◽  
Vol 271 (6) ◽  
pp. R1654-R1659 ◽  
Author(s):  
U. Arnelo ◽  
J. Permert ◽  
T. E. Adrian ◽  
J. Larsson ◽  
P. Westermark ◽  
...  

Islet amyloid polypeptide (IAPP) is a hormonal peptide that at high doses has been shown to reduce food intake. In the present study, the dose-response effects of subcutaneous infusion of IAPP (0, 2, 7, and 25 pmol.kg-1.min-1) for 8 days on food intake and meal patterns in rats were investigated. At the end of the experiment, plasma was obtained and levels of IAPP were measured by radioimmunoassay. IAPP dose-dependently and transiently inhibited food intake. The minimal effective dose (2 pmol.kg-1.min-1) caused a small but significant (up to 14%, P < 0.01) inhibition of food intake that lasted 5 days. The highest dose administered (25 pmol.kg-1.min-1) had the greatest effect (up to 44%, P < 0.001), which lasted throughout the 8-day period. Reductions in feeding during light and dark phases occurred through a decrease in number of meals consumed rather than meal size or meal duration. IAPP also decreased body weight gain and water intake dose dependently. IAPP infusion of 2, 7, and 25 pmol.kg-1.min-1 increased plasma IAPP concentrations from a basal level of 10.3 +/- 0.7 pM to 35.1 +/- 5.4, 78.1 +/- 11.2, and 236.6 +/- 23.6 pM, respectively, values that are likely to be close to physiological and within the pathophysiological ranges. Thus IAPP may play an important physiological or pathophysiological role in control of food intake.


Appetite ◽  
2018 ◽  
Vol 131 ◽  
pp. 73-83 ◽  
Author(s):  
Danna Oomen ◽  
Maud Grol ◽  
Desiree Spronk ◽  
Charlotte Booth ◽  
Elaine Fox

2000 ◽  
Vol 2000 ◽  
pp. 22-22
Author(s):  
N.D. Cameron ◽  
J.C. Penman ◽  
E. McCullough

Leptin is synthesised and secreted from adipocytes into the blood stream and transported to the brain, where it acts to cause a release of factors which can reduce food intake (Houseknecht et al., 1998). There are two murine mutations of the recessive gene coding for leptin which are associated with obesity. The Lepob allele determines synthesis and secretion of leptin, while the Lepdb allele determines responsiveness to leptin. In the Edinburgh lean growth experiment in pigs, selection for high and low daily food intake (DFI) has been practiced for seven generations in a Large White herd, which provides the experimental resource to determine if the correlated response in fat deposition is consistent with insufficient leptin production or with insensitivity to leptin.


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