Impairment of gallbladder emptying in diabetes mellitus

Stone, Bradford G.; Gavaler, Judith S.; Belle, Steven H.; Shreiner, David P.; Peleman, Rene; Sarva, Rajendra P.; Yingvorapant, Nori; Thiel, David H. Van

doi:10.1016/0016-5085(88)90307-1

Cited by 120 publications

(65 citation statements)

References 24 publications

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“…Blood was taken at 2,4,6,8,10,12,16,19,22,25,30,40,50,70,90,135 and 180 min for immediate determination of glucose and later for plasma insulin measurements. In addition, three baseline samples were taken 15, 10 and 5 min before the glucose injection.…”

Section: Insulin Sensitivitymentioning

confidence: 99%

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Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

et al. 1998

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OBJECTIVE: To investigate whether total body fat mass or fat distribution and associated metabolic disturbances in glucose and lipid metabolism in¯uence the well known gallstone pathogenetic factors in obese subjects in order to explain why some obese subjects develop gallstones and some do not. DESIGN: Cross sectional study of gallstone pathogenetic factors, body composition, fat distribution, glucose and lipid metabolism. SUBJECTS: 57 healthy overweight subjects (aged 26±64 y, body mass index (BMI) 30±45 kg/m 2 ). MEASUREMENTS: Total and intra-abdominal fat masses were measured by dual X-ray absorptiometry and abdominal CT scanning, respectively. The lithogenic index was measured in aspirated bile. The gallbladder volume was determined by ultrasound and the gallbladder ejection fraction% by dynamic cholescintigraphy. Plasma cholecystokinin (CCK) concentrations during a meal were measured with a speci®c radioimmunoassay. Insulin sensitivity was measured by the Minimal Model and glucose tolerance by an oral glucose tolerance test (OGTT). Serum lipid concentrations were measured by standard methods. RESULTS: The gallbladder volume in the fasting state increased with increasing intra-abdominal fat mass (P 0.006) and was increased in subjects with impaired glucose tolerance (41 vs 27 ml, P 0.001). The lithogenic index was b 1 in all subjects and correlated with total fat mass (P 0.04). CONCLUSION: Gallstone pathogenesis in obesity seems to be in¯uenced by the total body fat mass and its regional distribution possibly via mutual association with the glucose tolerance.

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Section: Insulin Sensitivitymentioning

confidence: 99%

“…In diabetics without gallstone disease, emptying of the gallbladder is impaired 15 even when checking for obesity, 16 and the bile is supersaturated. 17 Cholecystokinin (CCK) regulates postprandial emptying 18 and, therefore, impaired contractility of the gallbladder might be caused by impaired release or receptor-binding of CCK.…”

Section: Introductionmentioning

confidence: 99%

Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

et al. 1998

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“…Fiorucci et al [10] have shown that CCK-induced gallbladder contraction in diabetic patients, even in patients with autonomic neuropathy, was not significantly different from control subjects. Stone et al [9] found that CCKinduced gallbladder contraction in diabetic patients without neuropathy was not impaired, whereas in diabetic patients with autonomic neuropathy gallbladder contraction was significantly reduced. Using a meal as a stimulus, instead of CCK infusion, most investigators agree that gallbladder emptying in diabetic patients with autonomic neuropathy is reduced [6,7].…”

Section: Discussionmentioning

confidence: 99%

“…In the studies reporting a reduced gallbladder contraction in response to CCK in diabetic patients, actual blood glucose concentrations during the study period were not recorded [8,9]. In the study of Stone et al [9] no correlation was found between impaired gallbladder emptying in diabetic patients and overall glycaemic control as determined HbAlc levels. However, in the present study we have shown that during a hyperglycaemia of 15 mmol/1 the gallbladder contraction in response to infusion of 0.25 IDU-kg-1.…”

Section: Discussionmentioning

confidence: 99%

“…Although previous studies have shown that gallbladder emptying is impaired in patients with diabetes [6][7][8][9], in other studies gallbladder contraction in diabetic patients was not significantly different from control subjects [10,11]. It has been suggested that impaired gallbladder emptying in diabetes is related to the presence of autonomic neuropathy [6,9,10].…”

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confidence: 97%

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Effect of hyperglycaemia on gallbladder motility in Type 1 (insulin-dependent) diabetes mellitus

et al. 1994

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SummaryPatients with diabetes mellitus are at increased risk of developing gallstones. This has been attributed, among other factors, to alterations in gallbladder motility in the presence of autonomic neuropathy. Since high blood glucose concentrations impair gastric emptying in diabetic patients, we have investigated the effect of acute hyperglycaemia on gallbladder motility. Seven Type 1 (insulin-dependent) diabetic patients were studied twice during euglycaemia (blood glucose 5 mmol/1) and hyperglycaemia (blood glucose 15 mmol/1) using a clamp technique. In addition, seven healthy volunteers were studied during euglycaemia and hyperglycaemia. Gallbladder volumes, measured with ultrasonography, were studied before and during infusion of step-wise increasing doses of cholecystokinin-33, 0.25, 0.5 and 1.0 Ivy Dog Unit. kg-1. h-1, each dose for 30 min. Mean basal gallbladder volumes were not significantly different in the four experiments. Administration of cholecystokinin resulted in significant (p < 0.05) dose-dependent reductions in gallbladder volume in all experiments. During euglycaemia the gallbladder contraction in diabetic patients was not significantly different from the control subjects. During hyperglycaemia the gallbladder contraction in the diabetic patients was significantly (p < 0.05) reduced compared to euglycaemia only during infusion of 0.25 Ivy Dog Unit-kg -1. h-1 of cholecystokinin (19 + 6 % vs 33 + 6 %). Compared to euglycaemia, during hyperglycaemia the gallbladder contraction in the control subjects was significantly (p < 0.05) reduced during infusion of 0.25, 0.5 and 1.0 Ivy Dog Unit-kg-~-h -1 of cholecystokinin (14+4% vs 31+3%; 42+6% vs 65 + 5 % ; 74 _+ 4 % vs 90 +_ 3 %, respectively). It is concluded that during euglycaemia the gallbladder contraction in response to cholecystokinin in Type 1 diabetic patients is not significantly different from control subjects. During hyperglycaemia the gallbladder contraction in response to 0.25 Ivy Dog Unit. kg-1. h-1 cholecystokinin, leading to cholecystokinin levels as observed after ingestion of a light meal, is significantly reduced in Type i diabetic patients. [Diabetologia (1994) 37: 75-81]

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Management of Gallstones in Diabetic Patients

Aucott

Cooper²,

Bloom

et al. 1993

Arch Intern Med

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The management of gallstones in diabetic patients has traditionally been considered problematic. Autopsy findings and uncontrolled studies have documented a higher prevalence of cholelithiasis in diabetics, and early reports showed dramatically increased perioperative morbidity and mortality for treatment of diabetics with acute cholecystitis. As a result, some authorities have recommended prophylactic cholecystectomy for diabetic patients with asymptomatic gallstones, which is in contrast to recommendations for nondiabetics. More recent investigators have shown comparable rates of operative morbidity and mortality for biliary surgery in diabetics when compared with the general population. Recent studies have questioned whether diabetes is an independent risk factor for gallstone formation. Decision analyses using these new data have shown that prophylactic cholecystectomy is not of clear benefit and should not be routinely recommended for diabetics with asymptomatic gallstones. We believe that available data, although limited, indicate that asymptomatic patients with diabetes do not benefit from screening for gallstones and that cholecystectomy should only be performed in cases of symptomatic cholelithiasis, as is the case in the general population.

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Impairment of gallbladder emptying in diabetes mellitus

Cited by 120 publications

References 24 publications

Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

Fasting gall bladder volume and lithogenicity in relation to glucose tolerance, total and intra-abdominal fat masses in obese non-diabetic subjects

Effect of hyperglycaemia on gallbladder motility in Type 1 (insulin-dependent) diabetes mellitus

Management of Gallstones in Diabetic Patients

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