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Beyond preventing deficiency, research suggests that higher therapeutic doses of methylcobalamin may actively support nerve repair and regeneration

This change in available IGF-1 may be (it is difficult to extrapolate data from altered IGF-1/GH concentrations from animal models, as each author measures IGF-1 levels using different methods) adequate for fatty acid (FA) oxidation in muscle, suppression of GH, stimulation of glucose transport into muscle [171, 172], and lastly for the suppression of renal gluconeogenesis in mice [163]

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