1. Somatostatin analogues, such as SMS 201–995 (sandostatin), have been suggested as treatment for a variety of disease states including acromegaly, secretory gastrointestinal tumours and diabetes mellitus.

2. Somatostatin-14 has actions to prolong gastrointestinal transit time and inhibit intestinal absorption, and we have therefore studied the effects of SMS 201–995 on these processes. Five male subjects received a test meal having been given either saline or 50 μg of SMS 201–995 subcutaneously 30 min before ingestion.

3. SMS 201–995 caused a delay in mouth-to-caecum transit time for lactulose assessed by breath hydrogen analysis (316 ± 17 vs 192 ± 14 min, mean ±sem, P < 0.01), a delay (234 vs 120 min, P < 0.05) in the plasma peak of the non-metabolizable glucose analogue 3-O-methylglucose and conversion of the expected postprandial rise in serum triglycerides (with saline 1.02 ± 0.20 to 1.51 ± 0.28 mmol/l, P < 0.05) to a decrease below basal values (with SMS 201–995 0.97 ±0.80 to 0.79 ± 0.11 mmol/l, P < 0.05).

4. After SMS 201–995, an enhancement of the increase in blood glucose (8.2 ±0.7 vs 4.7 ±0.2 mmol/l, P < 0.01) and inhibition and postponement of the postprandial rise in insulin (27.6 ±6.7 vs 9.9 ±2.1 m-units/l, P < 0.05) occurred. Furthermore, a rise in non-esterified fatty acids, glycerol and 3-hydroxybutyrate, compared with the decline in concentrations of these metabolites after saline, was observed.

5. We conclude that SMS 201–995 has actions to increase mouth-to-caecum transit time, to diminish the rate of active monosaccharide absorption and to lower basal and postprandial triglyceride levels. These effects probably relate to inhibition of exo- and endo-crine gastrointestinal secretion.

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