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

The dynamics of the placental lactogenic hormone level, insulin requirements, and glycaemia during pregnancy was studied in diabetes I and II patients and diabetic pregnancies. Fructose amine and C-peptide levels in maternal and neonatal blood were measured in different diabetes types. The risk of diabetes I development in relation to the incidence of the HLA-system antigens was assessed. The need for a functional insulin therapy prior to and during pregnancy was substantiated.
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PMID:[Pregnancy and diabetes mellitus]. 275 80

Fructose is credited with some advantages over sucrose: it causes less of an increment in plasma glucose and insulin response, and the taste is sweeter. We reevaluated the latter property with a new methodology (the "up and down" method adapted from Dixon) in 33 healthy subjects, 17 insulin-dependent diabetes mellitus (IDDM) patients, and 12 non-insulin-dependent diabetes mellitus (NIDDM) patients. Sweetening potency was determined over 2-3 test sessions in each subject. Results are expressed in percent as the relative sweetness (R) of fructose (F) over sucrose (S), taken as reference. In the first set of experiments, with a 30-g/L sucrose-water solution at pH 7, we found that R values were similar for healthy subjects (102 +/- 8%) and diabetic subjects (106 +/- 7%) (P less than .05). No significant difference between IDDM and NIDDM patients was observed. In a second set of experiments, performed in healthy subjects only, R was increased in acid water (114%; P less than .01), in lemon juice (136%; P less than .001), in water at 2 degrees C (130%; P less than .001), and in coffee at 2 degrees C (120%; P less than .02); mean values were decreased in grapefruit juice (77%; P less than .001), in water at 43 degrees C (88%; P less than .01), and in coffee at 53 degrees C (87%; P less than .001). We found that the test methodology had a very satisfactory intrasubject reproducibility (coefficient of variation [C.V.] less than 8%) but a very wide intersubject variability (C.V. congruent to 32%).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Relative sweetness of fructose compared with sucrose in healthy and diabetic subjects. 275 52

Exogenously induced hyperinsulinemia can increase in vivo triglyceride production in rats receiving dietary fructose, either as monosaccharide or as sucrose, but not in those receiving only glucose. Thus, in the presence of fructose, but not glucose, insulin stimulates triglyceride production. Dietary fructose can also impair the removal of circulating triglyceride. Exogenous insulin overcomes this fructose-associated impairment of triglyceride removal. On the other hand, streptozotocin-diabetic rats showed a suppressed triglyceride secretion rate (TgSR) but their plasma triglyceride level was unchanged. Therefore, insulin deficiency may result in not only decreased production of triglyceride but also impaired triglyceride removal from the circulation. Fructose-fed diabetic rats showed higher plasma triglyceride levels than chow-fed diabetic rats without a concomitant increase in TgSR, suggesting impaired triglyceride removal from the circulation induced by fructose in diabetic rats. Glucose-fed diabetic rats did not differ in TgSR or plasma triglyceride level from chow-fed diabetic rats. These observations indicate that circulating insulin and dietary fructose, but not glucose, have a key role in very-low-density lipoprotein triglyceride turnover in rats.
Diabetes Res Clin Pract 1989
PMID:The role of insulin in triglyceride turnover in rats. 280 54

The effects of glucose and diabetes on the high-affinity lofentanil-displaceable opiate-receptor binding in mouse brain membranes were studied to determine if the attenuation of opiate actions by hyperglycemia previously observed in our laboratory was due to a modification of receptor affinity or number. With membranes from normal ICR mice, glucose (100-400 mg/dl) caused small but significant concentration-dependent decreases in receptor affinities for [3H]naloxone and [3H]dihydromorphine, both in the absence and presence of 20 mM NaCl, without changing the maximum number of binding sites. Fructose and the nonmetabolizable sugar 3-O-methylglucose had intermediate effects on naloxone affinity in the presence of NaCl that were not significantly different from control or from the effect of glucose. Similar results were obtained with brain membranes from streptozocin-induced diabetic mice. The binding affinity for [3H]naloxone in the presence of NaCl was not affected by the induction of diabetes in ICR mice via streptozocin or in spontaneously diabetic (db/db) C57BL/KsJ mice compared with their nondiabetic (m+/m+) littermates. These results indicate that the previously observed attenuation of opiate effects by glucose may be partly due to a glucose-induced decrease in opiate-receptor affinity. However, the much greater attenuation of morphine by fructose in vivo cannot be explained by this mechanism.
Diabetes 1987 Oct
PMID:Effects of glucose and diabetes on binding of naloxone and dihydromorphine to opiate receptors in mouse brain. 282 Aug 20

Fructose raises blood glucose and lactate levels in normal as well as diabetic man, but the tissue origin (liver and/or kidney) of these responses and the role of insulin in determining the end products of fructose metabolism have not been fully established. Splanchnic and renal substrate exchange was therefore examined during intravenous infusion of fructose or saline in six insulin-deficient type I diabetics who fasted overnight and in five healthy controls. Fructose infusion resulted in similar arterial concentrations and regional uptake of fructose in the two groups. Splanchnic glucose output increased threefold in the diabetics but remained unchanged in controls in response to fructose infusion, and the arterial glucose concentration rose more in diabetics (+5.5 mmol/liter) than in controls (+0.5 mmol/liter). Splanchnic uptake of both lactate and pyruvate increased twofold in response to fructose infusion in the diabetics. In contrast, a consistent splanchnic release of both lactate and pyruvate was seen during fructose infusion in controls. In diabetics fructose-induced hyperglycemia was associated with no net renal glucose exchange, while there was a significant renal glucose production during fructose infusion in the controls. In both groups fructose infusion resulted in renal output of lactate and pyruvate. In the diabetics this release corresponded to the augmented uptake by splanchnic tissues. In two diabetic patients given insulin infusion, all responses to fructose infusion were normalized. Fructose infusion in diabetics did not influence either splanchnic ketone body production or its relationship to splanchnic FFA inflow. We conclude that in insulin-deficient, mildly ketotic type I diabetes, (a) both the liver, by virtue of lactate, pyruvate, and fructose-derived gluconeogenesis, and the kidneys , by virtue of fructose-derived lactate and pyruvate production, contribute to fructose-induced hyperglycemia; (b) outcome of hepatic fructose metabolism; and (c) fructose does not exert an antiketogenic effect. These data suggest that while total fructose metabolism is not altered in diabetics, intermediary hepatic fructose metabolism is dependent on the presence of insulin.
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PMID:Splanchnic and renal exchange of infused fructose in insulin-deficient type 1 diabetic patients and healthy controls. 291 Sep 19

This study examined the hypothesis that the glucose component of food and not the total carbohydrate is the major determinant of the glycemic response in patients with insulin-dependent diabetes mellitus. Patients were given glucose alone, fructose alone, glucose + fructose, lactose, and glucose + fat + protein. Fructose given alone increased the blood glucose almost as much as a similar amount of glucose (78% of the glucose-alone area, p less than 0.05). However, the same amount of fructose given with glucose produced no greater glycemic response than did glucose alone (108%). Similarly, galactose contributed only slightly to the glycemic response when given as lactose (122%, p less than 0.01) whereas protein and fat had no additional glycemic effect (101%). To test the above hypothesis in natural foods, patients were fed an amount of bread (high glycemic index) or apple (low glycemic index) that contained 25 g glucose. Both challenges produced glycemic responses very similar to 25 g purified glucose.
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PMID:Glycemic responses in insulin-dependent diabetic patients: effect of food composition. 259 39

Fructose has been considered as an alternative sweetener to sucrose because it results in less glycemia when given to normal subjects or to those with mild noninsulin-dependent diabetes mellitus. Oral fructose also results in efficient glycogen synthesis. However, multiple hepatotoxic effects have been reported following parenteral fructose administration. We have examined the effects of large oral fructose and glucose loads (4 g/kg) and of graded intravenous fructose doses (50-500 mg/kg) on hepatic metabolism and glycogen synthesis in normal, fasted rats. Fructose was absorbed more slowly than glucose when given by gavage (59% vs 91% absorbed in 120 min). Oral fructose administration resulted in greater liver and muscle glycogen synthesis, despite smaller increases in plasma glucose and insulin concentrations, than was found after oral glucose administration. Increases in percent glycogen synthase I (active form) occurred after both oral fructose and glucose loads (67% vs 115% increase). There was no evidence of hepatotoxicity even after a very large oral fructose load. When small (less than or equal to 125 mg/kg) iv doses of fructose were given, the portal vein fructose concentration remained less than or equal to that found after oral fructose administration (1.1 mM). The percent synthase I increased up to threefold, and there was no evidence of hepatotoxicity. Larger iv doses resulted in a fall in percent synthase I, an increase in percent phosphorylase a, and inorganic phosphate and nucleotide depletion. We conclude that the slow absorption of an oral fructose load prevents hepatotoxic effects and permits efficient glycogen synthesis.
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PMID:Metabolic effects of dietary versus parenteral fructose. 309 1

In rat hepatocytes, the basal glycogen synthase activation state is decreased in the fed and diabetic states, whereas glycogen phosphorylase a activity decreases only in diabetes. Diabetes practically abolishes the time- and dose-dependent activation of glycogen synthase to glucose especially in the fed state. Fructose, however, is still able to activate this enzyme. Glycogen phosphorylase response to both sugars is operative in all cases. Cell incubation with the combination of 20 mM glucose plus 3 mM fructose produces a great activation of glycogen synthase and a potentiated glycogen deposition in both normal and diabetic conditions. Using radiolabeled sugars, we demonstrate that this enhanced glycogen synthesis is achieved from both glucose and fructose even in the diabetic state. Therefore, the presence of fructose plays a permissive role in glycogen synthesis from glucose in diabetic animals. Glucose and fructose increase the intracellular concentration of glucose 6-phosphate and fructose reduces the concentration of ATP. There is a close correlation between the ratio of the intracellular concentrations of glucose 6-phosphate and ATP (G6-P/ATP) and the activation state of glycogen synthase in hepatocytes from both normal and diabetic animals. However, for any given value of the G6-P/ATP ratio, the activation state of glycogen synthase in diabetic animals is always lower than that of normal animals. This suggests that the system that activates glycogen synthase (synthase phosphatase activity) is impaired in the diabetic state. The permissive effect of fructose is probably exerted through its capacity to increase the G6-P/ATP ratio which may partially increase synthase phosphatase activity, rendering glycogen synthase active.
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PMID:Glycogen synthesis from glucose and fructose in hepatocytes from diabetic rats. 314 17

The effects of a daily intake of 30 g fructose on blood glucose regulation, erythrocyte insulin receptors, and lipid metabolism have been studied in type II (non-insulin-dependent) diabetic subjects. Eight well-controlled patients received, in a randomly assigned crossover design over two 2-mo study periods, 30 g of fructose in exchange for an isocaloric amount of starch. Fructose could be taken at any time during the day as part of the 1400-1600 kcal allowed diet (50% carbohydrate, 30% fat, 20% protein). No significant difference was observed concerning body weight, HbA1c, fasting plasma glucose, fasting plasma insulin, uric acid, total cholesterol, high-density lipoprotein cholesterol, and triglycerides, nor was there any change in insulin binding to erythrocytes between the fructose and the control starch period. However, the mean plasma triglyceride levels after the fructose period, although still in the normal range, were significantly higher than baseline values (P less than .05). We conclude that moderate amounts of fructose incorporated into the diet of well-controlled type II diabetic subjects have no significant deleterious effect on glycemic control, insulin receptors of erythrocytes, or lipid metabolism.
Diabetes Care
PMID:Lack of detectable deleterious effects on metabolic control of daily fructose ingestion for 2 mo in NIDDM patients. 320 71

Fructose has a reaction constant 7.5 times as high as that of glucose in its nonenzymatic reaction with protein in vitro. The effects of glucose, sucrose and fructose ingestion on serum fructose and glucose levels were studied to evaluate the overall biohazard, i.e., the probability of their altering proteins while circulating in the blood. Normal and diabetic subjects were given either 75 g glucose, 75 g fructose, 75 g sucrose, or 112.5 g fructose after fasting, and their serum levels of sugars were measured at 0, 1, 2 and 3 h. In normal subjects, fructose ingestion produced significantly lower serum glucose levels and significantly higher serum fructose levels than did glucose ingestion, while sucrose produced intermediate results. The glycemic effect was found to be lowest for fructose and highest for glucose. The calculated overall biohazard was, however, highest for fructose and lowest for glucose in normal subjects. Furthermore, the serum fructosemic index was directly proportional to the amount of fructose ingested. In diabetic subjects, blood fructose clearance was significantly more delayed than in the controls when the same amount of fructose was ingested. These results suggest that an evaluation of the effects of simple in the diabetic diet requires a closer examination of the overall biological effects of the sugars.
Diabetes Res Clin Pract 1988 Apr 06
PMID:Effects of several simple sugars on serum glucose and serum fructose levels in normal and diabetic subjects. 337 Nov 78


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