Effect of Somatostatin on Intestinal Motility

Efendić, Suad; Mattsson, Ove

doi:10.1177/028418517801900209

Cited by 36 publications

(7 citation statements)

References 4 publications

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“…Nonetheless, there is strong indirect evidence that the principal mechanism for the increased percentage of deoxycholic acid in the bile of patients with octreotide‐associated gall‐bladder stones is prolongation of intestinal transit. Thus, several previous studies have reported that both native somatostatin 60–63 and its analogue octreotide 35 , 64–68 prolong mouth‐to‐caecum transit times. In paired, before and during treatment, studies of acromegalic patients, we also showed 67 that the mean colonic transit time increased by approximately 15 h, with an associated linear increase in serum deoxycholic acid (expressed as a percentage of serum total bile acids).…”

Section: Discussionmentioning

confidence: 98%

Octreotide increases the proportions of arachidonic acid‐rich phospholipids in gall‐bladder bile

Pereira

Hussaini

Murphy

et al. 2001

Aliment Pharmacol Ther

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Background and aims: Octreotide treatment of acromegalic patients induces cholesterol gallstone formation, in part by impairing cholecystokinin release and gall‐bladder contraction. However, there are few data on the effect of octreotide on biliary arachidonic acid‐rich phospholipids or mucin glycoprotein, factors which also influence cholesterol gallstone formation. Methods: In acromegalic patients studied before and during 3 months of octreotide treatment, we measured mucin glycoprotein concentrations and the molecular species of phosphatidylcholine, and related the results to the cholesterol saturation and percentage of deoxycholic acid in gall‐bladder bile. Results: The relative proportions of the major arachidonic acid‐rich phosphatidylcholine species, PC 16:0–20:4 and PC 18:0–20:4, increased significantly during octreotide treatment. These changes were associated with a rise in the cholesterol saturation index and a non‐significant twofold increase in mucin glycoprotein concentration. There were significant correlations between PC 16:0–20:4 and the cholesterol saturation index, percentage of vesicular cholesterol and percentage of deoxycholic acid in gall‐bladder bile. Conclusions: In acromegalic patients, octreotide increases the proportions of arachidonic acid‐rich phospholipids, with associated rises in: (a) the cholesterol saturation index and percentage of vesicular cholesterol, and (b) the percentage of deoxycholic acid in gall‐bladder bile—changes similar to those found in patients with cholesterol‐rich gall‐bladder stones.

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Section: Discussionmentioning

confidence: 98%

Octreotide increases the proportions of arachidonic acid‐rich phospholipids in gall‐bladder bile

Pereira

Hussaini

Murphy

et al. 2001

Aliment Pharmacol Ther

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“…Also, because our patients have had diabetes for a mean of 16 yr, they may be more prone to develop subclinical autonomic visceral neuropathy. The latter could be aggravated by the known inhibitory effects of the analogue on Gl motility and nutrient absorption (46,47). Paradoxically, SMS 201-995 has been shown to be effective for intractable and life-threatening chronic diarrhea in a diabetic patient (48) and patients with watery-diarrhea-hypokalemic-achlorhydric syndrome due to vasoactive intestinal polypeptide-secreting tumor (49,50) and ileostomy (51).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Effects of Long-Acting Somatostatin Analogue (Sandostatin) in Type I Diabetic Patients on Conventional Therapy

Osei

O'Dorisio²,

Malarkey³

et al. 1989

Diabetes

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We evaluated the effectiveness of a more potent and longer-acting somatostatin analogue (SMS 201-995) as an adjunct to insulin therapy, in a double-blind placebo-controlled randomized study of 26 C-peptide-negative type I (insulin-dependent) diabetic patients (20 women, 6 men, aged 22-40 yr) on their conventional drug regimens for 12 wk. Eight patients received a low dose (10 micrograms) of the analogue, 9 received a high dose (50 micrograms) of the analogue, and 9 received placebo subcutaneously before breakfast and dinner. Twenty-four-hour serum glucose, free insulin, plasma growth hormone (GH), and glucagon profiles were obtained before and during treatment at 4-wk intervals. The mean age, duration of diabetes, daily insulin dose, and body weight were not significantly different among the groups. The mean weekly capillary blood glucose values and exogenous insulin requirements were not changed by the SMS 201-995 therapy. Mean glycosylated hemoglobin A1 levels were unchanged in both the analogue- and placebo-treated groups at wk 12. Basal and postprandial glucose, free insulin, GH, and glucagon profiles were not influenced by the SMS 201-995 therapy throughout the study. Nocturnal glucose turnover rates (D-[3-3H]glucose technique) remained unaltered by the analogue therapy. Dose-dependent gastrointestinal (GI) adverse effects (e.g., diarrhea) were documented in the analogue-treated patients. Visual acuity and fundic photomicrographs of our patients were not changed by the analogue therapy. In conclusion, the prominent adverse GI effects our patients experienced preclude the use of larger doses of the analogue that may be necessary to suppress GH and glucagon and improve glucose control in type I diabetic patients.

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“…SP, which is known to increase intestinal transit (Liljedahl et al, 1958), was lower in the plasma of PCSK2-KO mice (Fig. 3A); whereas GLP-1, GLP-2 and SS, which are known to slow this transit (Bozkurt et al, 2002;Efendic and Mattsson, 1978), were higher (Fig. 3, panels B, C and D).…”

Section: Plasma Levels Of Neuroendocrine Peptidesmentioning

confidence: 96%

“…These include, among numerous others, the precursors of cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and GLP-2, neuropeptide Y (NPY), peptide YY (PYY), somatostatin (SS) and substance P (SP). SP stimulates GI motility (Niel, 1991), whereas CCK, GLP-1, GLP-2 and SS inhibit it (Anvari et al, 1998;Bozkurt et al, 2002;Efendic and Mattsson, 1978;Grider, 1994;von der Ohe et al, 1992). NPY stimulates appetite (Lynch et al, 1994), whereas PYY and GLP-1 reduce it (McMahon and Wellman, 1998;Ueno et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

PCSK2-null mice exhibit delayed intestinal motility, reduced refeeding response and altered plasma levels of several regulatory peptides

et al. 2011

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Effect of Somatostatin on Intestinal Motility

Cited by 36 publications

References 4 publications

Octreotide increases the proportions of arachidonic acid‐rich phospholipids in gall‐bladder bile

Octreotide increases the proportions of arachidonic acid‐rich phospholipids in gall‐bladder bile

Metabolic Effects of Long-Acting Somatostatin Analogue (Sandostatin) in Type I Diabetic Patients on Conventional Therapy

PCSK2-null mice exhibit delayed intestinal motility, reduced refeeding response and altered plasma levels of several regulatory peptides

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