Increased disaccharidase activity in human diabetics

Tandon, R. P.; Lm, Srivastava; Pandey, Sonika

doi:10.1093/ajcn/28.6.621

Cited by 38 publications

(20 citation statements)

References 18 publications

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“…For example, experimental diabetes has been reported to increase the enzymatic activity of many brush border hydrolases including the disaccharidases (1)(2)(3)(4) and to stimulate a number of transport systems believed to reside in this membrane (5)(6)(7)(8)(9)(10). Diabetes mellitus in man has also been associated with increased intestinal disaccharidase activity (11,12) and enhanced glucose absorption (13), although negative studies in man have also been reported (14,15) perhaps because of differing severity of the disease and effects of treatrnent. We have examined the effects of experimental diabetes on the metabolism of a representative brush border membrane enzyme, sucrase, to obtain some insight into the mechanism of the increased function of this membrane in diabetes.…”

Section: Introductionmentioning

confidence: 99%

The Intestinal Brush Border Membrane in Diabetes

Olsen¹,

Korsmo²

1977

J. Clin. Invest.

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A B S T R A C T Diabetes stimulates the functional activity of the intestinal brush border membrane with enhancement of both hydrolytic enzyme activity and membrane transport systems. To determine the mechanism of this effect, we studied the effects of streptozotocin diabetes on the metabolism of one membrane protein, sucrase-isomaltase, which increases its activity in diabetes. The protein was purified and an antiserum prepared. Sucrase-isomaltase from control and diabetic rats was immunologically identical as shown by Ouchterlony double-diffusion analysis of papainsolubilized mucosal proteins. The increase in sucrase enzyme activity in diabetic animals (31.0±1.4 U SEM 5 days after streptozotocin vs. 13.1±1.0 in controls) was the consequence of increased enzyme protein and not an alteration in catalytic efficiency as demonstrated by quantitative immunoprecipitin reactions.To account for increased sucrase-isomaltase protein in diabetes we studied papain-solubilized mucosal proteins labeled by injection of [14C]carbonate and[14C]leucine and analyzed incorporation into sucraseisomaltase protein (anti-serum precipitable) and total protein (trichloroacetic acid precipitable). We found that diabetes did not affect the decay of labeled total protein, but prolonged the decay of labeled sucraseisomaltase. t4 of sucrase-isomaltase was 4.4 h in control animals after [14C]carbonate injection and 8.8 and 10.2 h, respectively, 2 and 5 days after induction of streptozotocin diabetes. We obtained similar results in experiments with [14C]leucine with diabetes increasing t4 from 6 to 13.6 h. Diabetes did not appear to increase the rate of addition of sucrase-isomaltase to the brush border membrane, since it did not affect the 10-and 60-min incorporations of isotope into sucraseReceived for publication 11 January 1977 and in revised form 16 March 1977. isomaltase protein relative to incorporation into total protein and did not alter rate constants for synthesis calculated from the ti and the change in enzyme mass over time.Thus, enhanced sucrase activity in the diabetic animal is the consequence of an increase in sucraseisomaltase protein which develops because of a decrease in its rate of degradation. INTRODUCTIONInsulin deficiency stimulates the functional activity of the brush border membrane of the intestinal absorptive cell. For example, experimental diabetes has been reported to increase the enzymatic activity of many brush border hydrolases including the disaccharidases (1-4) and to stimulate a number of transport systems believed to reside in this membrane (5-10). Diabetes mellitus in man has also been associated with increased intestinal disaccharidase activity (11, 12) and enhanced glucose absorption (13), although negative studies in man have also been reported (14, 15) perhaps because of differing severity of the disease and effects of treatrnent. We have examined the effects of experimental diabetes on the metabolism of a representative brush border membrane enzyme, sucrase, to obtain some insight into the mechani...

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Section: Introductionmentioning

confidence: 99%

The Intestinal Brush Border Membrane in Diabetes

Olsen¹,

Korsmo²

1977

J. Clin. Invest.

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“…LM can be manifested clinically as lactose intolerance (LI) by flatulence, bloating, distension, diarrhoea and abdominal pain, causing many people to avoid drinking milk (Birge et al, 1967). In humans, intestinal lactase activity is increased in diabetes and has been shown to normalise on insulin treatment (Tandon et al, 1975). Furthermore, milk lipids containing high amounts of energy might contribute to obesity and an increased risk for diabetes.…”

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confidence: 99%

The genetic variant of lactase persistence C (−13910) T as a risk factor for type I and II diabetes in the Finnish population

et al. 2004

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Objective: Lactase persistence (LP), the ability to maintain a high lactase activity throughout life, has been suggested to be a possible risk factor for diabetes. Recently, a single nucleotide polymorphism C (À13910) T, residing 14 kb from the 5 0 end of the lactase (LCT) gene was shown to be associated with LP. Here we have studied the relationship between C (13910) T polymorphism and diabetes in the Finnish population. Patients and design: In all, 1455 patients with type I and 615 with type II diabetes and 446 nondiabetic controls in the Finnish population were genotyped for the C (-13910) T polymorphism by PCR minisequencing. Results: No differences were detected in the LP genotype frequencies (CT&TT) between diabetic and nondiabetic subjects. Conclusions: We conclude that the C (À13910) T polymorphism associated with lifelong LP is not a risk factor for type I or type II diabetes in the Finnish population.

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“…Disaccharidase activity has been shown to be increased in diabetic patients. 8) Further, in various diabetic model animals, hyperplasia of the intestinal mucosa has been reported. 6,7) As a result, the production of glucose and its absorption in the small intestine increases remarkably in the diabetic condition and may amplify the blood glucose level.…”

Section: Discussionmentioning

confidence: 98%

“…6,8) In the model rats, the jejunal mucosal weights of the STZ group were increased by approximately 2-fold when compared with that of the control group. Further, the increment in the mucosal weights of the intestinal segments was coupled to the increase in the DNA contents of the same segments.…”

Section: Discussionmentioning

confidence: 99%

“…1,4,5) Moreover, intestinal mucosal hypertrophy 6,7) and the related increase in disaccharidase activity is observed in both animals and humans. 8,9) It is reported that one of the traditional Kampo prescriptions, namely, Hachimi-jio-gan (HJ), has an antidiabetic action that ameliorates hyperglycemia and protects against diabetic nephropathy in experimental diabetic model rats. 10,11) In this study, we examined the eŠects of HJ on intestinal function using streptozotocin (STZ)-induced diabetic model rats.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Hachimi-jio-gan (Ba-Wei-Di-Huang-Wan) on Intestinal Function in Streptozotocin-induced Diabetic Rats

Hirotani

Ikeda

et al. 2007

YAKUGAKU ZASSHI

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We examined the eŠects of Hachimi-jio-gan (HJ) on the small intestinal function in streptozotocin (STZ)-induced diabetic rats. The rats had free access to pellets containing 1％ HJ extract powder for 4 weeks after STZ administration. The intestinal disaccharidase (sucrase and maltase) activity was elevated in STZ-treated rats compared with control rats, whereas it was signiˆcantly reduced by HJ administration. This suggested that HJ suppresses or delays monosaccharide production in the small intestinal epithelium. In addition, the intestinal mucosal weights and DNA contents that were signiˆcantly increased in the STZ-treated rats were restrained to the control level by HJ treatment. Simultaneously, we examined the changes in the plasma levels of glucagon-like peptide 2 (GLP-2), which is a trophic factor speciˆc for the intestine. The plasma GLP-2 levels signiˆcantly increased in the STZ-treated rats, whereas HJ decreased the plasma GLP-2 levels. Thus intestinal mucosal weights and DNA contents correlated with plasma GLP-2 levels in diabetes-associated bowel growth. These results suggest that HJ may normalize or suppress the small intestinal disaccharidase activity and the epithelial cell proliferation mediated by GLP-2 in the animal model rats.

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Increased disaccharidase activity in human diabetics

Cited by 38 publications

References 18 publications

The Intestinal Brush Border Membrane in Diabetes

The Intestinal Brush Border Membrane in Diabetes

The genetic variant of lactase persistence C (−13910) T as a risk factor for type I and II diabetes in the Finnish population

Effects of Hachimi-jio-gan (Ba-Wei-Di-Huang-Wan) on Intestinal Function in Streptozotocin-induced Diabetic Rats

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