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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood gastrin, sugar, insulin and glucagon were studied after a protein meal with or without 400 mg cymethidine per os in 7 normal subjects and 14 with anacidotic adult diabetes in a reasonable state of glycometabolic compensation. The association led to a significant enhancement of gastrin after 120' and 180', plus a rise in the total integrated gastrin response. Sugar and insulin were unaffected, while glucagon was distinclty, though not signifacantly, reduced. In a discussion of the results it is suggested that the rise in gastrin after cymethidine is not solely due to a pH-dependent negative feedback, since this should have led to an earlier (30', 60') rise, but also to the slight suppression of glucagon, which is physiologically endowed with the ability to inhibit secretion.
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PMID:[Behavior of gastrinemia, insulinemia and glucagonemia in normal and diabetic subjects after a protein meal accompanied by cimetidine]. 677 96

Sucrose, sorbitol, and fructose (35 g) were fed to normal and diabetic subjects as a component of a 400-calorie breakfast. In both normal and diabetic subjects, the mean peak increment in plasma glucose was highest after the sucrose meals (44.0 mg/dl for normal subjects; 78.0 mg/dl for diabetic subjects); lowest after sorbitol meals (9.3 mg/dl for normal subjects; 32.3 mg/dl for diabetic subjects); and intermediate after the fructose meals (29.0 mg/dl for normal subjects; 48.0 mg/dl for diabetic subjects). In normal subjects, the mean peak increment of plasma immunoreactive insulin followed a similar pattern, but in diabetic subjects there was no significant difference between the three groups. We conclude that fructose or sorbitol, given as part of a meal, results in lower glucose levels in both normal and diabetic subjects, but that the latter is not related to a difference in insulin release.
Diabetes Care
PMID:A comparison of carbohydrate metabolism after sucrose, sorbitol, and fructose meals in normal and diabetic subjects. 700 12

Sucrose consumption is a controversial issue. Part of the difficulty arises because of inadequate knowledge about the actual consumption of populations, as well as individuals within a population. Data on the sucrose content of foods are lacking. This review presents information published in the 1970s on these topics as well as current research and thinking about possible relationships of sucrose consumption to dental caries, cardiovascular disease, diabetes, obesity, and other disease conditions. Current attitudes toward recommendations concerning sugar consumption in the U.S. Dietary Goals are examined, as are data on the use of sugar as a fortification vehicle.
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PMID:The nutrition significance of sucrose consumption, 1970-1980. 700 64

Two groups of rats were fed diets in which the carbohydrate components was either starch or sucrose. A third group was fed on a stock diet. Half of the animals in each group were made diabetic by injection of either streptozotocin, in two of the groups, or alloxan, in the third group. Both diabetes and sucrose-feeding increased renal gluconeogenesis as indicated by increased activities of fructose-1,6-diphosphatase and glucose-6-phosphatase. Sucrose-feeding increased fatty acid synthesis both in the liver and kidney. However, the effect of diabetes on fatty acid synthesis was different at the two tissue sites. Diabetes, whether induced by streptozotocin or alloxan, decreased fatty acid synthesis in the liver but increased the rate in the kidney. The latter response was obtained for each diet but was additive with the effect of sucrose. We conclude that the effect of diabetes on renal lipid metabolism may reflect, in part, the accelerated glucose flux. The response to both diabetes and sucrose-feeding is also possibly associated with the increased lipid required for the membrane synthesis reported previously.
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PMID:Changes in metabolism of rat kidney and liver caused by experimental diabetes and by dietary sucrose. 709 29

In order to determine whether the fructose moiety of sucrose or the lack of some factor essential for the integrity of the microvascular system was responsible for the development of sucrose retinopathy in the rat, a series of diets containing possible sources of such a factor and/or fructose was tested over a 6-mo period. Examination of the isolated rat retinal vascular systems showed conclusively that fructose was the dietary microangiopathic agent associated with sucrose-induced retinopathy. The microvascular lesions produced were similar to those found in diabetic rats maintained over the same period. Cross-sectional studies of the retinas revealed that microvascular lesions preceded the associated degeneration of neural tissue rather than vice versa since the majority of rats with retinopathy showed no signs of neural damage. Sucrose feeding was found to produce a significant elevation (p < 0.001) in blood fructose concentration and a slight increase, albeit not significant (p < 0.01), in retinal fructose-1-phosphate (F1P) levels. The results are discussed in relation to the changes in retinal sorbitol, fructose, FIP, and lactate metabolism found in diabetes.
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PMID:Identification of fructose as the retinopathic agent associated with the ingestion of sucrose-rich diets in the rat. 745 69

The present study was designed to determine the possible significance of a therapeutic dose (0.2 mg) of AO-128 on carbohydrate absorption by measuring the breath hydrogen concentration, which is an index of the amount of unabsorbed carbohydrate in the large intestine. Post-prandial hyperglycemia is common among diabetic patients. AO-128, a potent alpha-glucosidase inhibitor, suppressed post-prandial hyperglycemia and hyperinsulinemia in healthy volunteers at a dose of 0.2 mg with each meal. These volunteers increased the breath hydrogen concentration in response to ingestion of non-absorbable lactulose, but decreased only slightly its concentration from the basal level after sucrose ingestion, indicating complete absorption. When AO-128 (0.2 mg) was given with sucrose, hydrogen production increased only slightly compared with placebo, suggesting that the inhibitory effect of AO-128 on sucrose absorption was minimal. Only 5 g of the 100 g of sucrose was not absorbed and this 5% reduction is too small to explain the observed inhibitory effect on the post-prandial rise in plasma glucose. Sucrose loading in rats (about 443 mg) sharply increased blood glucose and was accompanied by the rapid disappearance of sucrose from the upper small intestine. AO-128 (0.03 or 0.1 mg/kg) lessened the elevation of blood glucose after sucrose ingestion. The lower dose (0.03 mg/kg) retarded small intestinal absorption, but did not induce an influx of sucrose into the cecum and large intestine, while the higher dose (0.1 mg/kg) caused an increased influx of sucrose into the large bowel. These results indicated that AO-128 retards the absorption of carbohydrate and reduces post-prandial hyperglycemia.
Diabetes Res Clin Pract 1995 May
PMID:An alpha-glucosidase inhibitor, AO-128, retards carbohydrate absorption in rats and humans. 758 23

We evaluated the course of diabetes and nephropathy in the SHR/N-cp (corpulent) rat characterized by genetic obesity, non-insulin-dependent diabetes (NIDDM), and hypertension, and examined whether the nephropathy in this model is influenced by the type of carbohydrate intake. Two groups of obese and lean SHR/N-cp rats were fed diets containing 54% carbohydrate, as either sucrose or starch for 3 months (group I) and 9 months (group II). After 3 months on either diet, group I obese rats had higher 2-h response serum glucose levels and urinary glucose excretion than lean rats. Sucrose feeding was associated with greater proteinuria and a higher percentage of abnormal glomeruli in obese rats. Morphometric evaluation of glomeruli (by computerized image analysis) showed greater mean renal corpuscular volume and mesangial fraction in obese than in lean rats fed similar diets. Mean renal corpuscular volume and mesangial fraction were also greater in sucrose-fed obese rats than in starch-fed obese rats. After 9 months, group II obese rats had substantial reductions in serum and urine glucose levels but they were still hyperinsulinaemic and showed more proteinuria than lean rats and a higher percentage of sclerotic glomeruli compared with group I obese rats. At this time, mean mesangial fraction but not renal corpuscular volume was still higher in obese than in lean rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diabetic glomerulopathy in the SHR/N-corpulent rat: role of dietary carbohydrate in a model of NIDDM. 774 27

Studies were done to compare the acute effects of streptozotocin-induced diabetes and sucrose consumption on micturition, bladder mass and contractile responses of bladder strips to field stimulation and contractile agonists. Micturition changes occurred gradually in diabetic rats, reached maximal values within 7 to 14 days, and were accompanied by significant increases in bladder mass after 7 days. Bladder strips from diabetics responded to field stimulation, carbachol and KCl with significantly greater contractions than did those from controls within 7 days. Sucrose-drinking rats had maximal increases in fluid consumption and micturition frequency on the first night after starting treatment. Increases in micturition volumes were slower to develop than in diabetics. Bladder mass was significantly increased 30 and 60 days after starting sucrose treatment. Bladder strips from sucrose-drinking rats responded to field stimulation and carbachol with significantly greater contractions than did those from controls only after 60 days. Monitoring of drinking and micturition patterns established that diabetic rats drink and urinate during both the dark and light cycles. In contrast, control and sucrose-drinking rats drink and urinate principally at night. The results demonstrate that differences in bladder function between diabetic and sucrose drinking rats are apparent during the first month after treatment begins. The data suggest that the effects of diabetes and sucrose consumption on contractile bladder function are related to the diuresis-induced increases in bladder mass.
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PMID:Temporal changes in micturition and bladder contractility after sucrose diuresis and streptozotocin-induced diabetes mellitus in rats. 775 86

1. The responses of bladder strips from control, streptozotocin-diabetic, and sucrose-drinking rats to electrical field stimulation were investigated. Sucrose-drinking rats were included as additional controls because they have enlarged bladders as a result of non-diabetic diuresis. 2. Bladder strips from diabetic rats developed more spontaneous activity than those from the two control groups. Indomethacin reduced the amplitude and frequency of spontaneous contractions suggesting that they resulted from endogenous prostaglandin formation. Tetrodotoxin (TTX) had little effect, while alpha, beta-methylene ATP caused increases in spontaneous activity. 3. Bladder strips from diabetic rats responded to field stimulation with greater contractions than controls in the absence of antagonists as well as in the presence of atropine and alpha, beta-methylene ATP. Increasing TTX concentrations caused a step-wise depression of the contractile response to electrical stimulation which was not affected by preincubation with either atropine or alpha, beta-methylene ATP. 4. Atropine and indomethacin had no effect on strength-duration curves constructed to measure threshold contractile responses to five pulses stimulation. The curves were shifted to the right by both TTX and alpha, beta-methylene ATP, indicating that the responses were neurogenic in nature and at least partially, the result of stimulation of P2-purinoceptors. In the absence of drugs, bladder strips from diabetics responded at lower voltages and pulse widths than those of control and sucrose-drinking rats, suggesting that they were more excitable. 5. The response curve of bladder strips from diabetics to field stimulation at increasing voltage was shifted upwards and to the left compared to strips from control or sucrose-drinking rats. 6. Bladder strips from diabetics responded to stimulation at increasing pulse width with greater responses than those from control or sucrose-drinking rats. At 1.0 ms pulse width, the TTX-resistant response of strips from diabetic rats was still greater than that of the other groups, indicating that a myogenic component was also involved.7. The data suggest that bladder strips from diabetic rats are more excitable than those of control or sucrose-drinking rats. This may result from diabetes-induced decreases in bladder lipid or other membrane changes, and/or be a result of partial depolarization, perhaps related to diabetic neuropathy.
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PMID:Factors underlying the increased sensitivity to field stimulation of urinary bladder strips from streptozotocin-induced diabetic rats. 781 10

The eSS rat is a model of human spontaneous non-insulin-dependent diabetes. Male eSS rats were divided at the age of 4 months into two groups (eSSA and eSSB), both receiving the usual commercial balanced diet with sucrose also made available to eSSA. Sucrose intake did not imply a higher caloric diet, and no differences were found between groups in body weight and plasma triglyceride levels from 6 to 12 months of age. Sucrose option resulted in lower protein, lipid and carbohydrate intakes in eSSA animals. Plasma glucose values were higher in eSSA at different times of the tolerance curve. Likewise, eSSA kidneys showed significantly higher capsular and glomerular diameters and there was a discrete PAS-positive thickening of their basement membrane. We conclude that prolonged ad libitum sucrose intake, without weight gain, causes a moderate metabolic impairment and renal lesions in the eSS diabetic rat.
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PMID:Effects of dietary sucrose option on the diabetic syndrome of the eSS rat. 796 Jun 89


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