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Lipid absorption, distribution, and clearance also were equivalent with genotypes exhibiting identical serum triglyceride kinetics in the absence or presence of tyloxapol (Figure 4, B and C), which inhibits lipoprotein lipase-mediated triglyceride uptake by peripheral tissues ().

Additionally, the transcripts of rate-limiting proteins mediating lipid absorption (Fabp2), glucose absorption (Glut2, Sglt1), fatty acid and triglyceride synthesis (Fasn, Dgat1, Dgat2), and fatty acid oxidation (Acadm, Acadl) were equally expressed in intestines of the genotypes (Figure 4D).

(F) Correlation of fasted serum leptin level and body weight of 12-month-old mice raised on HCD (r mice were hyperphagic, independent of sex, dietary nutrients, or dietary caloric content (Figure 3A).

In that context, body masses of the genotypes were reversibly equalized by pair feeding (Figure 3B), with a direct relationship between calories consumed and weight gained (Figure 3C).

Points represent the mean of 10 daily food intake measurements (n = 10 per group).

(B) Growth of female mice pair-fed HCD (2.3 g/mouse/d) (n = 12).

Furthermore, GUCY2C deficiency amplified the metabolic syndrome associated with diet-induced obesity, including cardiac hypertrophy (Figure 2D), hyperleptinemia (Figure 2, E and F), hyperinsulinemia (Figure 2G), and impaired glycemic control (Figure 2H).

Moreover, the uroguanylin-GUCY2C endocrine axis may provide a therapeutic target to control appetite, obesity, and metabolic syndrome.

Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Phone: 215.955.6086, Fax: 215.955.7006, E-mail: Scott. Intestinal enteroendocrine cells are critical to central regulation of caloric consumption, since they activate hypothalamic circuits that decrease appetite and thereby restrict meal size by secreting hormones in response to nutrients in the gut.

Although guanylyl cyclase and downstream c GMP are essential regulators of centrally regulated feeding behavior in invertebrates, the role of this primordial signaling mechanism in mammalian appetite regulation has eluded definition.

Of significance, differential food consumption between genotypes was amplified by fasting, independent of dietary caloric content or nutrient composition (Figure 3D), suggesting impaired satiation.

Indeed, fasted and refed Gucy2c (A) Daily food consumption of 3-month-old female and male mice fed MCD or HCD.

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