Decreased food intake and body weight in pancreatic polypeptide overexpressing mice

Ueno, Naohiko; Inui, Akio; Iwamoto, Masako; Yonenaga, Chika; Yuzuriha, H; Nagata, Toshiaki; Kaga, Toshihiro; Asakawa, Akihiro; Kasuga, Masato

doi:10.1016/s0016-5085(00)82860-7

Cited by 33 publications

(48 citation statements)

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“…Similar effects are observed in transgenic mice overexpressing PP (230) . The anorectic effect is mediated through Y4 receptors and is associated with reduced expression of NPY and orexin mRNA in the hypothalamus, being dependent on intact vagal signalling (229) .…”

Section: Pancreatic Polypeptidesupporting

confidence: 74%

Peripheral signalling involved in energy homeostasis control

2012

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The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY 3 -36 , produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

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Section: Pancreatic Polypeptidesupporting

confidence: 74%

Peripheral signalling involved in energy homeostasis control

2012

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“…One of these hormones is peptide YY (PYY), which belongs to a family of peptides including neuropeptide Y (NPY) and pancreatic polypeptide (PP), all of which are known to have potent effects on feeding and energy balance via their unique interactions with G-protein-coupled Y receptors (Y1, Y2, Y4, Y5, y6) (Blomqvist and Herzog, 1997, Stanley et al, 1986and Ueno et al, 1999.…”

Section: Introductionmentioning

confidence: 99%

PYY transgenic mice are protected against diet-induced and genetic obesity

et al. 2008

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The gut-derived hormone, peptide YY (PYY) reduces food intake and enhances satiety in both humans and animals. Obese individuals also have a deficiency in circulating peptide YY, although whether this is a cause or a consequence of obesity is unclear. Our aims were to determine whether peptide YY (PYY) over-expression may have therapeutic effects for the treatment of obesity by altering energy balance and glucose homeostasis. We generated PYY transgenic mice and measured body weight, food intake, temperature, adiposity, glucose tolerance, circulating hormone and lipid concentrations and hypothalamic neuropeptide levels (neuropeptide Y; proopiomelanocortin, and thyrotropin-releasing hormone) under chow and high-fat feeding and after crossing these mice onto the genetically obese leptin-deficient ob/ob mouse background. PYY transgenic mice were protected against diet-induced obesity in association with increased body temperature (indicative of increased thermogenesis) and sustained expression of thyrotropin-releasing hormone in the paraventricular nucleus of the hypothalamus. Moreover, PYY transgenic mice crossed onto the genetically obese ob/ob background had significantly decreased weight gain and adiposity, reduced serum triglyceride levels and improved glucose tolerance compared to ob/ob controls. There was no effect of PYY transgenic over expression on basal or fastinginduced food intake measured at 11-12 weeks of age. Together, these findings suggest that long-term administration of PYY, PYY-like compounds or agents that stimulate PYY synthesis in vivo can reduce excess adiposity and improve glucose tolerance, possibly via effects on the hypothalamo-pituitary-thyroid axis and thermogenesis.

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“…11 Mice that overexpress PP have reduced weight gain and decreased food intake. 12 In humans, administration of pharmacological doses of PP has also been shown to decrease food intake over the following 24 h. 13,14 Furthermore, PP inhibits gastric emptying rate, exocrine pancreatic secretion and gallbladder motility. 15 In obese humans, studies concerning PP values have demonstrated conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Pancreatic polypeptide in obese children before and after weight loss

et al. 2006

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Objective: Little is known concerning pancreatic polypeptide (PP) in weight loss and in childhood obesity. Methods: Fasting PP, leptin and insulin concentrations were determined in 38 obese children and compared with 35 lean children of the same age, gender and pubertal stage. Furthermore, changes of PP concentrations over a 1-year period were analyzed in the obese children participating in a weight loss intervention program. Results: Obese children had significantly (Po0.01) lower PP, and higher leptin and insulin levels compared to lean children. In multiple linear regression analysis, PP was significantly negatively correlated to body mass index (Po0.01), but not to leptin, insulin, age, gender and pubertal stage. Changes of PP did not significantly correlate to changes of insulin (r ¼ 0.07, P ¼ 0.343) and leptin (r ¼ À0.02, P ¼ 0.459). The substantial weight loss in 17 children led to a significant (Po0.05) increase in PP and decrease in insulin and leptin. In the 21 children without substantial weight loss, there were no significant changes in PP, insulin and leptin. Conclusions: PP concentrations are decreased in obese children and independent of age, gender, pubertal stage, leptin and insulin. The decrease of PP in obese children normalized after weight loss. Therefore, low PP concentrations reflect the overweight status, rather than cause it.

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Decreased food intake and body weight in pancreatic polypeptide overexpressing mice

Cited by 33 publications

References 0 publications

Peripheral signalling involved in energy homeostasis control

Peripheral signalling involved in energy homeostasis control

PYY transgenic mice are protected against diet-induced and genetic obesity

Pancreatic polypeptide in obese children before and after weight loss

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