Abstract
Metabolically, hyperthyroidism is characterized by an increase in total energy expenditure and an augmented pulmonary oxygen uptake (1). There is also an increase in adipose tissue lipolysis (2,3) and net protein catabolism (4,5). This augmented mobilization of peripheral substrate depots is similar to that seen in fasting. In the fasted state, the liver plays an important metabolic role in converting the flux of amino acids and fatty acids into glucose and ketone bodies, respectively, thus supplying substrates that can be used by the central nervous system (6). The present study was undertaken to evaluate the effects of hyperthyroidism on splanchnic gluconeogenesis and ketogenesis.
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