Gastrointestinal Manifestations of Diabetes Mellitus

Taub, Sheldon J.; Mariani, A.; Barkin, Jamie S.

doi:10.2337/diacare.2.5.437

Cited by 32 publications

(13 citation statements)

References 49 publications

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“…Furthermore, the reduced output of pancreatic bicarbonate in human diabetic (3,4) suggests that pancreatic ductular functions as well as acinar function are abnormal. Unlike rats, most humans with diabetes do not have symptoms of severe pancreatic exocrine insufficiency such as steatorrhea (30,31); more detailed pancreatic function tests should be carried out in man to determine if the sensitivity to individual hormones (CCK and secretin) is altered as was the case for CCK in the present study in the diabetic rat.…”

Section: Discussionmentioning

confidence: 99%

“…It is not known whether this decreased pancreatic secretion is due to a decrease in the mass of normally functioning pancreatic acinar cells, a decrease in the content of specific digestive enzymes, a decrease in sensitivity to secretagogues or a combination of these factors. Many of the gastrointestinal manifestations of diabetes have previously been ascribed to diabetic neuropathy and autonomic insufficiency (30,31). Although it should not be assumed that all the changes in diabetes are due to insulin lack, pancreatic acinar cells are now known to be regulated directly by insulin; acinar cells possess specific insulin receptors and insulin is reported to increase glucose transport and protein synthesis by acini, and to potentiate the secretagogue action of CCK (16,26,(32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

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Effect of Diabetes Mellitus on the Regulation of Enzyme Secretion by Isolated Rat Pancreatic Acini

Ōtsuki¹,

Williams²

1982

J. Clin. Invest.

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A B S T R A C T The nature and mechanism of the pancreatic exocrine dysfunction in diabetes mellitus were evaluated in vitro using isolated pancreatic acini prepared from streptozotocin-induced diabetic rats. The content of amylase and ribonuclease in diabetic acini was -0.5 and 50% of the normal content, respectively. Further, reduced amounts of both enzymes were secreted by diabetic acini in response to both cholecystokinin (CCK) and carbamylcholine. However, when enzyme secretion was normalized relative to initial acinar contents, both normal and diabetic acini released enzymes at a comparable maximal rate. The time course of the release of these enzymes, and newly synthesized protein were similar in both acini. In normal acini, the effect of CCK was maximal at a concentration of 100 pM; higher concentrations led to submaximal enzyme release. The dose-response curve in diabetic acini was similarly shaped, but shifted threefold towards higher concentration. The mobilization of cellular Ca2" in response to CCK was also shifted.In contrast to these results with CCK, the dose-response curve to carbamylcholine was unaltered by diabetes. The observed effects were confirmed to be due to insulin deficiency and not due to direct toxic effect of streptozotocin on acinar cells or malnutrition. Streptozotocin had no acute effect on acini when measured 24 h after administration, and alloxan, another beta cell toxin, induced similar changes in acinar enzyme content and secretory response. Moreover, the administration of exogenous insulin to diabetic rats returned the content of pancreatic amylase and the secretory

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effect of Diabetes Mellitus on the Regulation of Enzyme Secretion by Isolated Rat Pancreatic Acini

Ōtsuki¹,

Williams²

1982

J. Clin. Invest.

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“…8 Diarrhea may occur continued anytime but usually is nocturnal and worse when the patient is supine. Patients may also experience postprandial exacerbations.…”

Section: Characteristic Findingsmentioning

confidence: 99%

Diabetic diarrhea

Beebe

Walley²

1992

Postgraduate Medicine

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Diarrhea is a common gastrointestinal problem in diabetes, and its prevalence has been underestimated. The cause of diabetic diarrhea is unknown, but it is probably related to gastrointestinal motility disturbances secondary to diabetic autonomic neuropathy. Other causes (especially primary malabsorption syndromes and islet cell tumors) must be excluded. Treatment of diabetic diarrhea is largely symptomatic and only moderately effective. Antidiarrheal agents may ameliorate acute episodes. Broad-spectrum antibiotics and clonidine hydrochloride (Catapres) have had some success in long-term control. Most recently, subcutaneous administration of somatostatin analogues has been shown to be helpful, the main side effects being drowsiness and vomiting.

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“…For this reason, gastric emptying should be as sessed in the diabetic with unexplained hypo glycemic reactions. Gastric stasis can also lead to bezoar formation [12], erratic absorption of oral medications, esophageal reflux [ 13], and, rarely, gastric bacterial overgrowth and/or gastric candidiasis [9]. The signs and symp toms of gastroparesis are nonspecific and may resemble reflux esophagitis, peptic ulcer dis ease, uremia, or medication side effects.…”

Section: Clinical Presentationmentioning

confidence: 99%

“…When symptoms are present, they may include anorexia, nausea, vomiting, ab dominal pain, early satiety, heartburn, bloat ing, halitosis, and weight loss [5,7,8]. Vomitus may contain food ingested several hours earlier [4], The duration of symptoms is vari able and may last for several weeks or may be of short duration separated by symptom-free intervals [8,9]. There is no correlation be tween gastric emptying by radiolabeled scinti graphy and upper gastrointestinal symptoms in diabetics with gastroparesis [6,10,11].…”

Section: Clinical Presentationmentioning

confidence: 99%

Diabetic Gastroparesis

Farell¹,

Keeffe²

1995

Dig Dis

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Diabetic gastroparesis is a common, underrecognized disorder affecting both type I and type II diabetics usually in the setting of other diabetic complications. The pathogenesis of diabetic gastroparesis is poorly understood, but autonomic neuropathy appears to play a major role. The symptoms of gastroparesis are nonspecific, and complications such as hypoglycemia and bezoar formation due to gastric stasis may occur. Diabetic gastroparesis can be assessed by measuring the gastric emptying of solid radiopaque markers or by scintigraphy. Treatment approaches include optimizing glycemic control and the use of prokinetic agents. Combination therapy or the alternating use of prokinetic agents may prove to be beneficial in dealing with drug tachyphylaxis.

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Gastrointestinal Manifestations of Diabetes Mellitus

Cited by 32 publications

References 49 publications

Effect of Diabetes Mellitus on the Regulation of Enzyme Secretion by Isolated Rat Pancreatic Acini

Effect of Diabetes Mellitus on the Regulation of Enzyme Secretion by Isolated Rat Pancreatic Acini

Diabetic diarrhea

Diabetic Gastroparesis

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