Diabetes and glucose transporter gene expression in rat small intestine

Miyamoto, Ken‐ichi; Hase, Kyoko; Taketani, Yutaka; Minami, Hisanori; Oka, Tatsuzo; Nakabou, Yukihiro; Hagihira, Hiroshi

doi:10.1016/0006-291x(91)92053-m

Cited by 72 publications

(55 citation statements)

References 24 publications

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“…Although the dual tracer approach used in the present experiments cannot distinguish between these two processes, the portal rate of appearance of enterically delivered glucose was slightly (but not significantly) lower in the diabetic subjects than in the nondiabetic subjects. This contrasts with reports that glucose absorption (25) and intestinal transport (49,50) are enhanced in chronically diabetic animals. Although this could be due to a species difference, it more likely is because the diabetic animals generally were severely hyperglycemic and hyperphagic, which presumably led to intestinal hypertrophy (51).…”

Section: Discussioncontrasting

confidence: 98%

Type 2 Diabetes Impairs Splanchnic Uptake of Glucose but Does Not Alter Intestinal Glucose Absorption During Enteral Glucose Feeding

et al. 2001

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We have previously reported that splanchnic glucose uptake, hepatic glycogen synthesis, and hepatic glucokinase activity are decreased in people with type 2 diabetes during intravenous glucose infusion. To determine whether these defects are also present during more physiological enteral glucose administration, we studied 11 diabetic and 14 nondiabetic volunteers using a combined organ catheterization-tracer infusion technique. Glucose was infused into the duodenum at a rate of 22 mol ⅐ kg ؊1 ⅐ min ؊1 while supplemental glucose was given intravenously to clamp glucose at ϳ10 mmol/l in both groups. Endogenous hormone secretion was inhibited with somatostatin, and insulin was infused to maintain plasma concentrations at ϳ300 pmol/l (i.e., twofold higher than our previous experiments). Total body glucose disappearance, splanchnic, and leg glucose extractions were markedly lower (P < 0.01) in the diabetic subjects than in the nondiabetic subjects. UDP-glucose flux, a measure of glycogen synthesis, was ϳ35% lower (P < 0.02) in the diabetic subjects than in the nondiabetic subjects. This was entirely accounted for by a decrease (P < 0.01) in the contribution of extracellular glucose because the contribution of the indirect pathway to hepatic glycogen synthesis was similar between groups. Neither endogenous and splanchnic glucose productions nor rates of appearance of the intraduodenally infused glucose in the portal vein differed between groups. In summary, both muscle and splanchnic glucose uptake are impaired in type 2 diabetes during enteral glucose administration. The defect in splanchnic glucose uptake appears to be due to decreased uptake of extracellular glucose, implying decreased glucokinase activity. Thus, abnormal hepatic and muscle (but not gut) glucose metabolism are likely to contribute to postprandial hyperglycemia in people with type 2 diabetes. Diabetes 50:1351-1362, 2001

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Section: Discussioncontrasting

confidence: 98%

Type 2 Diabetes Impairs Splanchnic Uptake of Glucose but Does Not Alter Intestinal Glucose Absorption During Enteral Glucose Feeding

et al. 2001

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“…The increment in intestinal SGLT1 mRNA in OLETF rats was considered to be independent of di-etary intake of carbohydrate since our study was undertaken in pair-feeding conditions. Both the SGLT1 and GLUT2 expression of the mRNA and protein contents were reported to be increased in the small intestine of streptozotocin-treated diabetic rats concomitant with increased glucose transport [34,35]. Although insulin deficiency, hyperphagia and hyperglycaemia could contribute to an increased expression of SGLT1 in those rats, the mechanism of the increased expression of transporters is unclear [35].…”

Section: Discussionmentioning

confidence: 99%

Increased intestinal glucose absorption and postprandial hyperglycaemia at the early step of glucose intolerance in Otsuka Long-Evans Tokushima Fatty Rats

et al. 1998

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Glucose intolerance is believed to be caused not only by insulin resistance but also impaired insulin secretion [1±3]. Dietary restrictions and exercise are effective in intervening in glucose intolerance, postprandial hyperglycaemia, and impaired insulin secretion [4,5]. a-glucosidase inhibitors, which delay intestinal glucose absorption, also improve postprandial hyperglycaemia and hyperinsulinaemia in Type II (non-insulin-dependent) diabetic patients [6] and prevent the progression from impaired glucose tolerance to Type II diabetes [7]. We therefore hypothesize that increased intestinal glucose absorption may be another possible factor regulating postprandial hyperglycaemia in diabetes mellitus. Diabetologia (1998) Summary Otsuka Long-Evans Tokushima Fatty (OLETF) rats are reported to be obese Type II (non-insulin-dependent) diabetic rats with insulin resistance and impaired insulin secretion. To investigate the contribution of intestinal glucose absorption to postprandial hyperglycaemia, we determined the plasma xylose concentrations after an 0.8 g/kg oral xylose load which was used as a test of small intestinal glucose absorption in 6-week-old OLETF rats and weight-matched Long-Evans Tokushima Otsuka (LETO) rats. An oral glucose tolerance test showed that OLETF rats developed hyperglycaemia at 60 and 90 min after the glucose load, though the fasting plasma glucose concentration, insulin concentration and insulin-induced in vivo glucose utilization rate were similar. Consistently, in an oral D-xylose loading test, the peak concentration of plasma xylose in OLETF rats was increased by 58.7 % compared with that of LETO rats (p < 0.005). The disappearance rate of plasma xylose concentrations after intravenous xylose loading did not differ between the two strains. Co-treatment with 0.4 g/kg phlorizin, a specific inhibitor of sodium-dependent glucose transporter 1 (SGLT1), abolished both plasma glucose and xylose concentrations after the loads. Morphological studies showed that both the small intestinal wet weight and surface area were 30 % larger in the OLETF rats than in the LETO rats. Furthermore, the SGLT1 mRNA content of OLETF rats also increased compared with LETO rats. These results suggest that an increased SGLT1 expression concomitant with intestinal hypertrophy in OLETF rats is partly associated with postprandial hyperglycaemia before the onset of insulin resistance and hyperinsulinaemia. [Diabetologia (1998

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“…Recent studies have found raised enterocyte levels of SGLT1 [4,5] and the facilitated transporter GLUT2 [5] in streptozotocin (STZ)-treated rats and increased expression of these proteins are now known to be involved in the enhanced glucose transport at the BBM and BLM, respectively.…”

Section: Animalsmentioning

confidence: 99%

Streptozotocin diabetes and the expression of GLUT1 at the brush border and basolateral membranes of intestinal enterocytes

et al. 1996

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Changes in membrane expression of sodium-dependent glucose transporter (SGLTI) and glucose transporter isoform (GLUT2) protein have been implicated in the increased intestinal glucose transport in streptozotocin-diabetes. The possible involvement of GLUT1 in the transport response, however, has not previously been studied. Using confocal microscopy on tissue sections and Western blotting of purified brush border membrane (BBM) and basolateral membrane (BLM), we have examined enterocyte expression of GLUTI in untreated and in 1 and 21 day streptozotocin diabetic rats. In control enterocytes, GLUT1 was absent at the BBM and detected at low levels at the BLM. Diabetes resulted in a 4-to 5-fold increased expression of GLUT1 at the BLM and the protein could also be readily detected at the BBM. Insulin treatment of diabetic rats increased GLUT1 level at the BBM but was without effect on expression of the protein at the BLM.

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Diabetes and glucose transporter gene expression in rat small intestine

Cited by 72 publications

References 24 publications

Type 2 Diabetes Impairs Splanchnic Uptake of Glucose but Does Not Alter Intestinal Glucose Absorption During Enteral Glucose Feeding

Type 2 Diabetes Impairs Splanchnic Uptake of Glucose but Does Not Alter Intestinal Glucose Absorption During Enteral Glucose Feeding

Increased intestinal glucose absorption and postprandial hyperglycaemia at the early step of glucose intolerance in Otsuka Long-Evans Tokushima Fatty Rats

Streptozotocin diabetes and the expression of GLUT1 at the brush border and basolateral membranes of intestinal enterocytes

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