Tissue Distribution and Excretion of Phenformin in Normal and Diabetic Animals

Hd, Hall; Gollamudi, Ramachander; Glassman, Jerome M.

doi:10.1111/j.1749-6632.1968.tb27734.x

Cited by 44 publications

(16 citation statements)

References 7 publications

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“…Biguanides have not been found to accumulate in the gastric mucosa [5] so a significant inhibition of the active transport systems in this region would not be expected. However, a significantly increased gastric acid output after the treatment period presumably involves stimulation of the parietal cell.…”

Section: Discussionmentioning

confidence: 99%

The effect of metformin treatment on gastric acid secretion and gastrointestinal hormone levels in normal subjects

1980

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Gastric acid secretion and gastrointestinal hormone levels were measured in healthy non-diabetic subjects after metformin treatment (1.5 g/day). The maximum acid output was increased from 15.7 +/- 3.9 mmol/h (mean +/- SEM) to 30.0 +/- 7.1 mmol/h (p < 0.05) and the peak acid output was increased from 16.4 +/- 4.1 mmol/h to 31.7 +/- 7.2 mmol/h (p < 0.05) after two weeks treatment. Serum insulin, gastric inhibitory polypeptide and secretin levels were normal. After treatment for one week, however, there was a significant increase in fasting vasoactive intestinal peptide (VIP) from 83 +/- 6 ng/1 to 102 +/- 9 ng/1 (p < 0.02) and in stimulated VIP from 58 +/- 5 ng/1 to 79 +/- 5 ng/1 (p < 0.05). Stimulated glucagon-like immunoreactivity (GLI) was also increased from 82 +/- 10 ng/1 to 174 +/- 24 ng/1 (p < 0.01) after one week's treatment. It is suggested that metformin acts as a weak histamine agonist.

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Section: Discussionmentioning

confidence: 99%

The effect of metformin treatment on gastric acid secretion and gastrointestinal hormone levels in normal subjects

1980

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“…It is apparently altered in the liver to an inert metabolite that, with the unchanged drug, is excreted in the urine. 11 We do not know how to inhibit the drug's action or speed its excretion or metabolic conversion, so treatment of pa-tients with phenfbrmin-associated lactic acidosis is limited to recognizing and treating coexisting lifethreatening disorders and to treating acidemia.…”

Section: Discussionmentioning

confidence: 99%

Phenformin-associated Metabolic Acidosis

Fulop

Hoberman

1976

Diabetes

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We report 18 consecutive phenformin-treated diabetic patients admitted to this Medical Service acutely ill with metabolic acidosis. Lactic acidosis was anticipated, and documented, in all. Also, however, though most of the patients had only weakly positive, or even negative, serum reactions with the nitroprusside reagent, all were found to have coexisting ketoacidosis, plasma 3-hydroxybutyrate averaging 7.1 mmol/L. +/- 3.9 (S.D.). This finding suggest that treatment of these patients should include insulin, and often also glucose, because most do not have marked hyperglycemia and some have hypoglycemia. The lactic acidosis in the nine patients who survivied was, on average, less severe than in the nine who died, but the difference was not statistically significant. Surivival correlated closely with the absence of shock on arrival. Only eight patients had a identifiable acute illness other than the metabolic acidosis. The other 10 patients had no discernible cause for the acute illness apart from their treatment with phenoformin. This finding raises serious doubts about whether phenformin should be used to treat patients with diabetes.

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“…It was noted in these studies that the excretion of sulfonamides was markedly influenced by urinary pH ; the more basic, the more rapid the sulfonamide excretion. Other drugs whose urinary excretion was investigated were phenformin, p-butoxyphenylacethydroxamic acid, anisotropine, and urea (1380)(1381)(1382)(1383)(1384). The excretion and metabolism of pheniramine, brompheniramine, amphetamine, phenobarbital, and metopimazine were the subject of various articles (1374)(1375)(1376)(1377)(1378)(1379).…”

Section: Bioph Arm Aceuticsmentioning

confidence: 99%