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 fasting-induced 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.
"Basal levels are lower and the meal-induced release of PYY 3–36 is blunted in obese individuals (Alvarez Bartolomé et al., 2002; Batterham et al., 2003; le Roux et al., 2006; Guo et al., 2006; Sodowski et al., 2007). Also, PYY overexpression protects against diet-induced obesity (Boey et al., 2008). Importantly, PYY 3–36 administration reduces food intake similarly in obese and non-obese subjects (Batterham et al., 2003; Sloth et al., 2007), implying that obesity does not decrease PYY 3–36 sensitivity. "
"Peptide YY (PYY) is a gut-brain anorexigenic hormone that promotes negative energy balance by reducing appetite . Peripheral infusion of PYY reduces food intake in rodents , and transgenic mice overexpressing PYY have increased plasma PYY concentrations, and are protected against diet-induced obesity . "
[Show abstract][Hide abstract] ABSTRACT: A low-grade pro-inflammatory state is at the pathogenic core of obesity and type 2 diabetes. We tested the hypothesis that the plant terpenoid compound ginsenoside Rb1 (Rb1), known to exert anti-inflammatory effects, would ameliorate obesity, obesity-associated inflammation and glucose intolerance in the high-fat diet-induced obese mouse model. Furthermore, we examined the effect of Rb1 treatment on central leptin sensitivity and the leptin signaling pathway in the hypothalamus. We found that intraperitoneal injections of Rb1 (14 mg/kg, daily) for 21 days significantly reduced body weight gain, fat mass accumulation, and improved glucose tolerance in obese mice on a HF diet compared to vehicle treatment. Importantly, Rb1 treatment also reduced levels of pro-inflammatory cytokines (TNF-α, IL-6 and/or IL-1β) and NF-κB pathway molecules (p-IKK and p-IκBα) in adipose tissue and liver. In the hypothalamus, Rb1 treatment decreased the expression of inflammatory markers (IL-6, IL-1β and p-IKK) and negative regulators of leptin signaling (SOCS3 and PTP1B). Furthermore, Rb1 treatment also restored the anorexic effect of leptin in high-fat fed mice as well as leptin pSTAT3 signaling in the hypothalamus. Ginsenoside Rb1 has potential for use as an anti-obesity therapeutic agent that modulates obesity-induced inflammation and improves central leptin sensitivity in HF diet-induced obesity.
PLoS ONE 03/2014; 9(3):e92618. DOI:10.1371/journal.pone.0092618 · 3.23 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: This study explored the dose-dependent effect of oat cereal β-glucan on improving metabolic indexes of obesity mice. C57-Bl mice were randomized to chow diet (N) group and high fat diet group and other three doses of oat β-glucan groups (low β-glucan, medium β-glucan, and high β-glucan). Energy intake, glucose, lipids, and appetite related hormones were tested. Dose-dependent relation was observed on oat β-glucan doses and body weight change, average energy intake, total cholesterol, HDL cholesterol, plasma neural peptide Y, arcuate neural peptide Y mRNA, and arcuate neural peptide Y receptor 2 mRNA level. Oat β-glucan helped to increase plasma peptide Y-Y and intestine peptide Y-Y expression in obesity mice.
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