Background Gallstone ileus is an important complication of cholecystolithiasis. In general, surgery is the treatment of choice for such cases, but clinicians face difficulty in the selection of an appropriate approach. Closure of a cholecystoenteric fistula can be achieved through one-stage or two-stage operation. Two-stage operation has a lower mortality rate than a one-stage procedure, but persistence of the cholecystoenteric fistula is associated with the risk of carcinogenesis and recurrence of gallstone ileus.Objective This study reviews the different surgical approaches according to the impaction site of the gallstone, using data of previous studies by our group and clinical reports in the literature.Conclusions First, for cases involving impaction at the duodenum, the cholecystoenteric fistula can be repaired in the same surgical field, and one-stage operation obtains favourable outcome; hence, one-stage operation is considered as treatment of choice. Second, for cases involving impaction at the small intestine, natural closure of the cholecystoenteric fistula or low mortality is expected; hence, two-stage operation may be performed, possibly using minimally invasive laparoscopy. Third, for cases involving impaction at the colon, natural closure of the cholecystocolonic fistula is unlikely, and patients have a high risk of reflux cholangitis due to faecal fluid; hence, one-stage operation is considered as treatment of choice.

Mutations in the mitochondrial gene were recently identified in a large pedigree of diabetes mellitus and deafness. As the mitochondrial gene is materially inherited, Japanese diabetic patients whose mothers were also diabetic were screened, using peripheral leucocytes, for an A to G transition at nucleotide pair 3243 of the mitochondrial gene, a tRNA(Leu(UUR)) mutation. This mutation was identified in four pedigrees from among 300 unrelated patients who were screened. Diabetes co-segregated with the mutation, except in one young subject, and was maternally inherited. The apparent onset of disease occurred between 11 and 68 years of age. Some of the affected members developed hearing impairment and congestive heart failure due to cardiomyopathy, though generally long after the onset of diabetes, and these patients had therefore not been diagnosed as having a specific form of diabetes. The duration of sulphonyl-urea treatment was not more than 8 years in these pedigrees and affected members were prone to progression to insulin-requiring diabetes. Thus, these patients were secondary sulphonylurea failures. Long-term follow-up revealed that the underlying disorder in affected members is a progressive impairment of insulin secretion. Some were initially diagnosed as having IDDM based on an apparent acute onset in youth and the clinical severity of their diabetes. Others were regarded as having MODY with an aggressive course. The mitochondrial gene mutation or diabetes is not transmitted to all offspring of the affected mothers.(ABSTRACT TRUNCATED AT 250 WORDS)

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To investigate the biological and biochemical properties of GLUT5, rat GLUT5 complementary DNA was transfected into Chinese hamster ovary cells. Rat GLUT5 was exclusively targeted to the plasma membrane and exhibited a transport activity, not for glucose, but for fructose. The affinity for fructose (Km = 11.6mM) was much higher than that of GLUT2, the other glucose transporter with fructose transport activity. Interestingly, rat GLUT5 was not photolabeled with 0.5 microM cytochalasin B, whereas a similar amount of GLUT1 was adequately photolabeled under the same experimental conditions. Next, to investigate the domains required for transport of glucose/fructose in GLUT1 and/or GLUT5, several chimeric GLUT1/GLUT5 proteins were expressed, and their glucose and/or fructose transport activities were studied. The intracellular middle loop and the region encompassing the membrane spanning domains 7-12 were observed to have crucial roles in GLUT1 glucose transport, whereas replacement of the N-terminal half or the intracellular C-terminal region with the corresponding region of GLUT5 produced no marked effects on glucose transport activity. In contrast, both the N-terminal half encompassing the region from the N-terminus through the 6th membrane spanning domain and the intracellular C-terminal region were mandatory for GLUT5 fructose transport. In conclusion, GLUT5 is a transporter exclusively for fructose and the structural requirements for fructose transport are more stringent than those for glucose transport among hexose transporter proteins.

We have isolated a clone from the rat jejunum cDNA library using a fragment of human GLUT5 cDNA as a probe. The coding region of this clone shares 80% nucleotide and 81% amino acid identity with human GLUT5 and is thus termed rat GLUT5 cDNA. Rat GLUT5 mRNA exhibited a tissue distribution very similar to that of human GLUT5, with the highest levels in the jejunum, but was not detected in fat, muscle, or testis on Northern blot analysis. The antipeptide antibody raised against the C-terminal domain of rat GLUT5 protein specifically recognized a rat jejunal protein with an apparent mol wt of 60,000 on immunoblots. The amount of GLUT5 mRNA and protein in the jejuni of rats fed a fructose-enriched diet (50%, wt/wt) for 3 days were increased 2.5- and 6-fold, respectively, compared to those of rats fed standard rat chow, whereas those of rats fed a starch-enriched diet (50%, wt/wt) were not altered. Similarly, GLUT5 mRNA and protein in the jejunum were increased 5- and 8-fold, respectively, after 15 days of fructose feeding. Thus, an increase in fructose absorption up-regulates GLUT5 expression in the jejunum. These results are consistent with the notion that GLUT5 plays a major role in fructose absorption in the small intestine.