Serotonin-transporter promoter polymorphism modulates the ability to control food intake: Effect on total weight loss

2017 ◽  
Vol 61 (11) ◽  
pp. 1700494 ◽  
Author(s):  
Gemma Bonnet ◽  
Purificación Gómez-Abellán ◽  
Beatriz Vera ◽  
Juan Francisco Sánchez-Romera ◽  
Antonio M. Hernández-Martínez ◽  
...  
Keyword(s):  
Weight Loss ◽  
Food Intake ◽  
Serotonin Transporter ◽  
Promoter Polymorphism ◽  
Total Weight ◽  
Total Weight Loss ◽  
Control Food ◽  
Serotonin Transporter Promoter Polymorphism ◽  
Control Food Intake

Parenteral nutrition, brain glycogen, and food intake

1993 ◽  
Vol 265 (6) ◽  
pp. R1387-R1391
Author(s):  
M. M. Meguid ◽  
J. L. Beverly ◽  
Z. J. Yang ◽  
J. R. Gleason ◽  
R. A. Meguid ◽  
...  
Keyword(s):  
Food Intake ◽  
Parenteral Nutrition ◽  
Plasma Glucose ◽  
Glycogen Content ◽  
Fischer 344 Rats ◽  
Brain Glycogen ◽  
Fischer 344 ◽  
Control Food ◽  
Control Food Intake ◽  
Infusion Period

To determine whether brain glycogen concentrations change during parenteral nutrition, Fischer 344 rats with jugular vein catheters received 0.9 N saline or parenteral nutrition providing 100% of daily calories (PN-100). Rats were killed after 4 days of PN-100 and serially after PN-100 was stopped. Food intake decreased during PN-100 to approximately 15% of control, but total kilocalories eaten and infused over the 4-day PN-100 period was approximately 130% of control. Food intake of PN-100 rats remained low for 3-4 days post-PN-100. At the end of the 4-day PN-100 period, plasma glucose and insulin (P = 0.01) and whole brain glycogen (P < 0.005) were higher than but similar to control within 24 h of PN-100 being stopped. When PN-100 rats were not allowed to eat during the infusion period, plasma glucose was lower, plasma insulin higher, and brain glycogen content the same as in control rats after 4 days of PN-100. The increased brain glycogen was the likely consequence of the hyperglycemia and hyperinsulinemia during PN-100 and was not causally associated with the reduced food intake either during or immediately after PN-100.

Low serum insulin-like growth factor-1 level is a predictor of low total weight loss percentage after sleeve gastrectomy

2020 ◽  
Vol 16 (12) ◽  
pp. 1978-1987
Author(s):  
Masahiro Ohira ◽  
Yasuhiro Watanabe ◽  
Takashi Yamaguchi ◽  
Atsuhito Saiki ◽  
Takashi Oshiro ◽  
...  
Keyword(s):  
Weight Loss ◽  
Sleeve Gastrectomy ◽  
Growth Factor ◽  
Serum Insulin ◽  
Total Weight ◽  
Total Weight Loss ◽  
Insulin Like Growth Factor ◽  
Weight Loss Percentage ◽  
Low Serum

scholarly journals Association between a serotonin transporter promoter polymorphism (5HTTLPR) and personality disorder traits in a community sample

2011 ◽  
Vol 45 (9) ◽  
pp. 1153-1159 ◽  
Author(s):  
Rianne M. Blom ◽  
Jack F. Samuels ◽  
Mark A. Riddle ◽  
O. Joseph Bienvenu ◽  
Marco A. Grados ◽  
...  
Keyword(s):  
Personality Disorder ◽  
Serotonin Transporter ◽  
Community Sample ◽  
Promoter Polymorphism ◽  
Serotonin Transporter Promoter Polymorphism

scholarly journals Peptide YY, appetite and food intake

2005 ◽  
Vol 64 (2) ◽  
pp. 213-216 ◽  
Author(s):  
C. W. le Roux ◽  
S. R. Bloom
Keyword(s):  
Food Intake ◽  
Peptide Yy ◽  
Energy Content ◽  
Peak Plasma ◽  
Evolutionary Relationship ◽  
Gut Hormones ◽  
Amino Acid Peptide ◽  
Control Food ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.

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