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(C) Correlation of mean daily food intake and weight gain of 4-month-old mice fed HCD during a 10-day period (r Beyond increased calorie consumption, excess adiposity may also reflect differences in digestion, nutrient absorption, and/or energy mobilization/expenditure.

In the context of the central role of dietary fat in obesity (), lipid digestion was identical between genotypes, and triglycerides were unmeasurable (completely digested), while free fatty acid levels were comparable in stool (Figure 4A).

(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).

The prohormone signal is selectively decoded in the hypothalamus by proteolytic liberation of uroguanylin, inducing GUCY2C signaling and consequent activation of downstream anorexigenic pathways.

Thus, evolutionary diversification of primitive guanylyl cyclase signaling pathways allows GUCY2C to coordinate endocrine regulation of central food acquisition pathways with paracrine control of intestinal homeostasis.

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

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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.

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The present study reveals that eliminating GUCY2C expression in mice disrupts appetite regulation specifically by impairing satiation, producing hyperphagia associated with comorbidities, including obesity and metabolic syndrome.

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