In animal models, subcutaneous neonatal MSG treatment induces
neuroendocrine obesity through hypothalamic lesion (Nakayama et al.,
2003; Xu et al., 2007) resulting in fat tissue accumulation, glucose intolerance,
hyperinsulinemia, and insulin resistance (Balbo et al., 2007). It has
been reported that obesity is not accompanied by hyperphagia (Martins
et al., 2004). Moreover, MSG treatment induces neuronal damage by
In animal models, subcutaneous neonatal MSG treatment inducesneuroendocrine obesity through hypothalamic lesion (Nakayama et al.,2003; Xu et al., 2007) resulting in fat tissue accumulation, glucose intolerance,hyperinsulinemia, and insulin resistance (Balbo et al., 2007). It hasbeen reported that obesity is not accompanied by hyperphagia (Martinset al., 2004). Moreover, MSG treatment induces neuronal damage by
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