Abstract

The glucose absorption inhibitors, Phenformin and 3-phenylpropylaminoguanide HCl (SaH 43–522) have different effects on hepatic gluconeogenesis. Unlike phenformin, 43–522 in vivo does not inhibit hepatic gluconeogenesis; inhibition occurred only when 43–522 was added directly to a liver perfusion system. This suggests that when 43–522 is administered in vivo it is metabolized to an agent that does not inhibit hepatic gluconeogenesis whereas phenformin is not metabolized, and does inhibit gluconeogenesis. This is an advantage of 43–522 since it thereby specifically inhibits intestinal glucose absorption without a potential hypoglycaemic effect due to the suppression of gluconeogenesis.

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