Carbohydrate Tolerance and Insulin Responses in Obstructive Jaundice

Soler, Norman G.; Exon, P.D.; Paton, Adrienne W.

doi:10.1136/bmj.4.5942.447

Cited by 17 publications

(5 citation statements)

References 10 publications

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“…In the present study, low insulin concentra tion, low ZAinsulin, and low XAinsulin/ZABG following glucose loading were found in the femoral blood of the jaundiced animals. These results confirm a previous ob servation [10] that a low insulin response following glu cose loading was often found in the peripheral venous blood in obstructive jaundice. Low SAinsulin and low ZAinsulin/ZABG were found in the portal blood of the jaundiced animals, suggesting that obstructive jaundice reduces insulin secretion from the pancreas in response to intraduodenal glucose loading.…”

Section: Discussionsupporting

confidence: 82%

“…Obstructive liver disease is, on the other hand, asso ciated with hypoinsulinemia in response to glucose load ing [10], and it is uncertain whether the hypoinsulinemia of the peripheral venous blood results from hyposecre- Table III tion from the pancreas or increased degradation of insu lin in the liver and peripheral tissue. We have, therefore, obtained blood samples not only from the femoral vein but also from the portal vein in which the level may be considered to represent the insulin secreted from the pancreas.…”

Section: Discussionmentioning

confidence: 99%

“…Glucose intolerance in liver disease has been well recognized since Naunyn first described what he called 'hepatogenous diabetes' [1]. It occurs commonly in cirrhosis [2][3][4], active chronic hepatitis [5], acute viral hepatitis [6], toxic hepatitis [7], and obstructive liver disease [8][9][10], Hyperinsulinemia af ter glucose loading appears to be associated with he patic cirrhosis [2,3,11], while hypoinsulinemia ap pears to be characteristic of obstructive liver disease [ 10].…”

Section: Introductionmentioning

confidence: 99%

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Glucose Tolerance and Insulin and Gastric Inhibitory Polypeptide Responses following Intraduodenal Glucose Loading in Dogs with Obstructive Jaundice

et al. 1987

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In order to elucidate the influence of bile duct obstruction on gastric inhibitory polypeptide (GIP) response, 7 anesthetized dogs were given an intraduodenal infusion of 1 g/kg glucose before and again 2 weeks after common bile duct ligation. Blood glucose and GIP responses following glucose loading of the jaundiced animals were significantly higher compared to the control animals in the femoral and portal blood but, nevertheless, the insulin responses were significantly lower not only in the femoral blood but also in the portal blood. These results suggest that bile duct obstruction causes a high GIP level and insulin hyposecretion resulting in abnormal glucose tolerance.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Glucose Tolerance and Insulin and Gastric Inhibitory Polypeptide Responses following Intraduodenal Glucose Loading in Dogs with Obstructive Jaundice

et al. 1987

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“…This is probably due to recent use of postoperative intraportal insulin administration in insulinopenic patients [32]. It is well known that glucose intolerance and impaired insulin secretion are often associated with obstructive jaundice [33,34]. This impairment is not fully reversed even after long-term PTBD [35], so postoperative management with great care is required in patients with insulinopenia due to obstructive jaundice.…”

Section: Discussionmentioning

confidence: 99%

Complications of Hepatectomy for Hilar Cholangiocarcinoma

et al. 2001

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We retrospectively reviewed postoperative complications in 105 patients with hilar cholangiocarcinoma who underwent hepatectomy at Nagoya University Hospital from January 1990 through March 1999. Of the 105 subjects, 97 (92.4%) underwent resection of two or more Healey's segments of the liver. Combined portal vein resection was performed in 33 (31.4%) patients and pancreatoduodenectomy in 10 (9.5%). Twenty (19.0%) patients had no postoperative complications, another 39 (37.1%) patients had minor complication(s) only, and the remaining 46 (43.8%) developed major complication(s). The morbidity rate reached as high as 81.0%. Major complications required relaparotomy in 11 (10.5%) patients. Of the 46 patients with major complication(s) 36 recovered; the remaining 10 patients died of liver failure with other organ failure(s) or of intraabdominal bleeding 12, 14, 18, 21, 57, 75, 75, 87, 93, or 134 days after surgery. Thus the 30-day mortality was 3.8% and the overall mortality 9.5%. Pleural effusion was the most frequent complication found in 66 (62.9%) patients, followed by wound sepsis in 39 (37.1%), and then liver failure in 29 (27.6%). Liver failure developed in 16.7% of 48 patients with less than 50% liver resection and in 36.8% of 57 patients with 50% or more resection (P < 0.05). Other organ failures, including renal, respiratory, gastrointestinal, and hematologic failures, developed as a sign of multiple organ failure following liver failure in most patients or preceding liver failure in a few patients. None of the six patients with four or more organ failures survived. Hepatectomy for hilar cholangiocarcinoma is risky owing to impaired hepatic functional reserve in jaundiced patients and the technical difficulty associated with hepatobiliary resection. Our goal is to reduce mortality to less than 5% while keeping a high resectability rate (above 80%).

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“…Both the kinetics changes and the lack of phosphorylation control are compatible with ischemia. ( Glucose intolerance accompanied by hypoinsulinemia has been observed in patients with obstructive jaundice (1) and in icteric rats (2, 3) and rabbits (3). Lowered fasted glucose levels (31, possibly caused by reduced liver gluconeogenesis (41, have also been observed in rats with experimentally induced cholestasis.…”

mentioning

confidence: 99%

Lack of Control of Liver Gluconeogenesis in Cholestatic Rats With Reduced Portal Blood Flow

1992

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Previous studies indicated a role for ischemia in the metabolic changes induced by cholestasis. Liver pyruvate kinase is a key enzyme for the concurrent control of glycolysis and gluconeogenesis. In this experiment the control of pyruvate kinase activity was investigated in cholestatic rats. Pyruvate kinase kinetics changed from a sigmoidal type in sham-operated rats to a hyperbolic type in obstructed rats. The change in the enzymatic kinetics paralleled the reduction in the portal blood flow, which reached 50% of the control value 7 days after obstruction. Dibutyryl cyclic AMP (5 mumol/kg body wt) plus theophylline 0.1 mmol/L failed to inactivate the enzyme when injected into the portal veins of rats whose livers were obstructed 7 days before. Both the kinetics changes and the lack of phosphorylation control are compatible with ischemia.

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Carbohydrate Tolerance and Insulin Responses in Obstructive Jaundice

Cited by 17 publications

References 10 publications

Glucose Tolerance and Insulin and Gastric Inhibitory Polypeptide Responses following Intraduodenal Glucose Loading in Dogs with Obstructive Jaundice

Glucose Tolerance and Insulin and Gastric Inhibitory Polypeptide Responses following Intraduodenal Glucose Loading in Dogs with Obstructive Jaundice

Complications of Hepatectomy for Hilar Cholangiocarcinoma

Lack of Control of Liver Gluconeogenesis in Cholestatic Rats With Reduced Portal Blood Flow

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