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PubMed1975

Glycerol intolerance in a child with intermittent hypoglycemia.

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.

Alanine↗
PubMed1980

[Glucose or sugar substitutes in parenteral infusions? The choice of carbohydrates in postoperative infusion therapy].

The aim of parenteral nutrition should be to optimise fluid, energy and nitrogen balance. In the post-traumatic or post-operative phase a stress induced glucose intolerance may occur and it may become difficult to meet the patient's energy requirements with glucose alone. For these reasons the use of sugar substitutes (fructose, sorbitol and xylitol) in combination with glucose is recommended as an alternative. Patients receiving a mixed sugar solution of glucose, fructose and xylitol at a ratio of 1:2:1 require less exogenous insulin and yet maintain a lower blood glucose concentration. Used in limited quantities, we encountered no side effects either in patients undergoing elective surgery or requiring intensive care.

Blood Glucose↗
PubMed1975

Protective effect of selenium on certain hepatotoxic and pancreotoxic manifestations of subacute cadmium administration.

Administration of cadmium chloride (1.0 mg/kg s.c.) to rats, twice a day for 7 days, significantly stimulated the activities of hepatic pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-diphosphatase and glucose 6-phosphatase, markedly increased the concentration of hepatic cyclic adenosine monophosphate and circulating blood glucose and significantly reduced serum insulin levels. Furthermore, subacute exposure to cadmium induced glucose intolerance that was associated with a decreased pancreatic secretory activity as evidenced by lowered insulinogenic indices and marked inhibition of phentolamine-stimulated insulin release. In contrast to cadmium, administration of selenium dioxide (2 X 1.0 mg/kg/day s.c., 7 days) failed to alter significantly the activities of gluconeogenic enzymes, hepatic cyclic adenosine monophosphate, blood glucose or serum insulin levels, glucose tolerance or the pancreatic secretory activity. However, administration of selenium concurrently with cadmium completely prevented the cadmium-induced increases of hepatic gluconeogenic enzymes. Treatment with selenium ameliorated the cadmium-induced hyperglycemia, hypoinsulinemia, glucose intolerance and the suppression of pancreatic secretory activity, whereas it failed to alter significantly the cadmium-induced elevation of hepatic cyclic AMP levels. Data provide evidence suggesting that subacute exposure to cadmium alters several parameters of carbohydrate metabolism and suppresses pancreatic secretory activity and that administration of selenium alone is without any appreciable effect on the above parameters. However, administration of selenium concurrently with cadmium prevents, to varying degrees, several of the cadmium-induced metabolic and functional changes.

Animals↗
PubMed1987

Metabolic effects of short-term fasting in obese hyperglycaemic humans and mice.

The aim of this study was to investigate the metabolic effects of short-term fasting in obese diabetic patients and to correlate the observed changes with the activity of hepatic key enzymes in an animal model of obesity-associated diabetes (ob/ob mice, C57BL/6J strain). In obese diabetic patients (ODP), a 72-h fast (causing slight change in body weight) decreased fasting glycemia by 3.82 +/- 0.79 mmoles/l and significantly improved glucose tolerance (OGTT) while reducing basal and stimulated insulinemia, whereas in obese non-diabetic patients (ONDP) only a small decrease in fasting glycemia (1.24 +/- 0.51 mmoles/l) occurred. This suggests that in ODP hyperphagia is a factor contributing to maintain hyperglycaemia and glucose intolerance (in the face of hyperinsulinaemia, indicating insulin resistance). In fed obese hyperglycaemic mice (OHM), which are a good model of the human obesity-associated diabetes, hepatic fructose-1,6-diphosphatase (F16Pase) and glucose-6-phosphatase (G6Pase), involved in glucose production, showed increased activity (+52 and +200 per cent, respectively) compared to control mice (CM), and the ratios of F16Pase and G6Pase to the opposing enzymes phosphofructokinase (PFK1) and glucokinase (GK), i.e. the F16Pase/PFK1 and G6Pase/GK ratios, were increased by 38 and 101 per cent, respectively, suggesting increase in gluconeogenesis and perhaps in glycogenolysis. In the 48-h fasted OHM, F16Pase activity was decreased (-30 per cent) compared to the fed animals, while the activity of G6Pase showed a smaller and statistically not significant change (-22 per cent). In contrast, in the CM a 48-h fasting was associated with a trend toward increased F16Pase (+22 per cent) and G6Pase (+173 per cent). However, since PFK1 and GK decreased to a similar extent in OHM and CM, the F16Pase/PFK1 and G6Pase/GK ratios, basally elevated in the OHM, did not change with fasting, whereas in the CM they showed a striking elevation (+71 and +274 per cent, respectively). The basally elevated F16Pase/PFK1 and G6Pase/GK ratios (functionally linked to glucose production) in the OHM may contribute to maintain hyperglycaemia; in these mice, the lack of further increase in the glucose production-related F16Pase/PFK1 and G6Pase/GK ratios (which occurs in CM) with fasting might allow that the interruption of the afflux of dietary carbohydrates ameliorates the glycaemic level. Similar mechanisms might occur also in the ODP.

Adult↗
PubMed1977

Disaccharide consumption and malabsorption in Canadian Indians.

Twenty-eight Sioux and 29 Saluteaux Indians from a southern and an isolated northern Manitoban community were screened for lactose malabsorption; 55 were also screened for sucrose tolerance. Sixty percent of the subjects were lactose malabsorbers; the incidence increased with age. Lactase deficiency appeared, on the average, between 8 and 15 years of age. About 45% of the subjects were lactose intolerant. Malabsorbers who did not regularly drink milk had the highest symptom scores. The northern subjects consumed significantly more lactose and sucrose than the southern subjects. Two Sioux children were sucrose malabsorbers. It was hypothesized that the significantly greater sucrose consumption by the Saulteaux subjects were responsible for their markedly higher blood glucose curve following the sucrose tolerance tests. Dietary sucrose increases jejunal sucrase activity and the intestinal transport of glucose and fructose. Three of eight children less than 4 years were lactose malabsorbers; hence, medical personnel treating noninjective diarrhea in Indian children should examine for lactase deficiency. It was recommended that vitamin D fortified milk supplements to Indian school children be continued and that the milk be treated so as to reduce abdominal symptoms in the intolerant individuals.

Adolescent↗
PubMed2000

Dietary P(i) deprivation in rats affects liver cAMP, glycogen, key steps of gluconeogenesis and glucose production.

We previously reported [Xie, Li, Méchin and van de Werve (1999) Biochem. J. 343, 393-396] that dietary phosphate deprivation for 2 days up-regulated both the catalytic subunit and the putative glucose-6-phosphate translocase of the rat liver microsomal glucose-6-phosphatase system, suggesting that increased hepatic glucose production might be responsible for the frequent clinical association of hypophosphataemia and glucose intolerance. We now show that liver cAMP was increased in rats fed with a diet deficient in P(i) compared with rats fed with a control diet. Accordingly, in the P(i)-deficient group pyruvate kinase was inactivated, the concentration of phosphoenolpyruvate was increased and fructose 2, 6-bisphosphate concentration was decreased. Phosphoenolpyruvate carboxykinase activity was marginally increased and glucokinase activity was unchanged by P(i) deprivation. The liver glycogen concentration decreased in the P(i)-deficient group. In the fed state, plasma glucose concentration was increased and plasma P(i) and insulin concentrations were substantially decreased in the P(i)-deficient group. All of these changes, except decreased plasma P(i), were cancelled in the overnight fasted P(i)-deficient group. In the fasted P(i)-deficient group, immediately after a glucose bolus, the plasma glucose level was elevated and the inhibition of endogenous glucose production was decreased. However, this mild glucose intolerance was not sufficient to affect the rate of fall of the glucose level after the glucose bolus. Taken together, these changes are compatible with a stimulation of liver gluconeogenesis and glycogenolysis by the P(i)-deficient diet and further indicate that the liver might contribute to impaired glucose homeostasis in P(i)-deficient states.

Animals↗
PubMed2006

Topiramate for smoking cessation.

Due to its AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)/kainate antagonism, topiramate would be particularly interesting in addiction treatment. Flexible-dose topiramate was prescribed to 13 smokers (10 smokers who wanted to stop smoking, and three who received topiramate for other reasons). Six out of 13 smokers were abstinent at 2 months and two more subjects had reduced their cigarette consumption by >50%. With one exception, temporary reduction of the number of smoked cigarettes preceded definitive abstinence at month 2. Three more subjects who achieved a momentary reduction had, however, to interrupt the treatment due to intolerable side-effects. Controlled trials are needed to confirm these preliminary observations.

Adult↗
PubMed1990

Comparison between a glucose-fructose-xylitol solution and a sole glucose solution for surgical patients with glucose tolerance impairment.

The metabolic response to the postoperative delivery of a sole glucose solution or a glucose-fructose-xylitol solution, and their effects upon carbohydrate metabolism, in patients with glucose tolerance impairment, were evaluated. Twenty four patients who showed an abnormal 75g-OGTT or were noninsulin-dependent diabetics were divided in two groups. The GFX-B group (n = 11) received a 10.5% solution, containing glucose, fructose and xylitol at 4:2:1 ratio, and the PHY-3 group (n = 13) received a 10% glucose solution, both, continuously infused for 3 days postoperatively. The infusion of PHY-3 tended to produce a higher increase in blood glucose than the infusion of GFX-B, that was significantly different on the 3POD (P less than 0.05). The increase in IRI and CPR was also significantly greater in PHY-3 group than in GFX-B group on the 3POD (P less than 0.05). We concluded that it was not only the slight lower glucose load of the GFX-B solution, but also, the different infused carbohydrate substrate which had influenced the magnitude of insulin secretion and the blood glucose level. Then, its use in glucose intolerant patients may be of some benefit to partially minimize the postoperative hyperglycemic response.

Adult↗
PubMed2006

Glucose metabolic adaptations in the intrauterine growth-restricted adult female rat offspring.

We studied glucose metabolic adaptations in the intrauterine growth-restricted (IUGR) rat offspring to decipher glucose homeostasis in metabolic programming. Glucose futile cycling (GFC), which is altered when there is imbalance between glucose production and utilization, was studied during a glucose tolerance test (GTT) in 2-day-old (n = 8), 2-mo-old (n = 22), and 15-mo-old (n = 22) female rat offspring. The IUGR rats exposed to either prenatal (CM/SP, n = 5 per age), postnatal (SM/CP, n = 6), or pre- and postnatal (SM/SP, n = 6) nutrient restriction were compared with age-matched controls (CM/CP, n = 5). At 2 days, IUGR pups (SP) were smaller and glucose intolerant and had increased hepatic glucose production and increased glucose disposal (P < 0.01) compared with controls (CP). At 2 mo, the GTT, glucose clearance, and GFC did not change. However, a decline in hepatic glucose-6-phosphatase (P < 0.05) and fructose-1,6-biphosphatase (P < 0.05) enzyme activities in the IUGR offspring was detected. At 15 mo, prenatal nutrient restriction (CM/SP) resulted in greater weight gain (P < 0.01) and hyperinsulinemia (P < 0.001) compared with postnatal nutrient restriction (SM/CP). A decline in GFC in the face of a normal GTT occurred in both the prenatal (CM/SP, P < 0.01) and postnatal calorie (SM/CP, P < 0.03) and growth-restricted offspring. The IUGR offspring with pre- and postnatal nutrient restriction (SM/SP) were smaller, hypoinsulinemic (P < 0.03), and hypoleptinemic (P < 0.03), with no change in GTT, hepatic glucose production, GFC, or glucose clearance. We conclude that there is pre- and postnatal programming that affects the postnatal compensatory adaptation of GFC and disposal initiated by changes in circulating insulin concentrations, thereby determining hepatic insulin sensitivity in a phenotype-specific manner.

Animals↗
PubMed1992

Metabolic abnormalities of the hyperglycemic obese Zucker rat.

In a cross-sectional study, we evaluated the metabolic profiles of lean (Fa/?) and obese (fa/fa) Zucker male rats at 4 to 8 months of age. Although all of the obese rats (N = 108) demonstrated glucose intolerance, most of the obese rats exhibited only mild elevations of fasted and fed plasma glucose. Only 14 of the obese rats were severely hyperglycemic, which resulted in substantial elevations of glycohemoglobin (GHb) levels. The nerve and lens levels of glucose, sorbitol, and fructose were elevated, and the myo-inositol was depleted in all hyperglycemic obese rats, but not in the euglycemic obese rats. With increasing duration of hyperglycemia, the neural myo-inositol level approached normal, while the lenses became cataractous. All obese rats had increased urinary albumin excretion (UAE), which was dependent on age (r = .45, P less than .02) and independent of hyperglycemia, glucosuria, and polyuria. In conclusion, although the euglycemic obese rats exhibited some diabetic abnormalities, the hyperglycemic obese Zucker rat more closely resembled the altered metabolic profile associated with type II diabetes mellitus.

Animals↗
PubMedDate not supplied

Efficacy of topiramate and valproate in chronic migraine.

OBJECTIVES: The aim of this study was to compare the efficacy of sodium valproate and topiramate in treating chronic migraine. METHODS: Forty-nine patients with chronic migraine were randomly assigned to 1 of 2 groups of treatment: 750 mg/day valproate or 75 mg/day topiramate. Efficacy variables were number of days with headache over a 30-day period and changes in Migraine Disability Assessment (MIDAS) scores at 3 months. RESULTS: At baseline the 2 groups had similar numbers of days with headache and mean MIDAS scores. At the end of the treatment period, a significant reduction in 30-day headache frequency with respect to baseline (P < 0.00001) and a significant reduction in MIDAS scores (P < 0.00001) were recorded in both groups. There were no significant differences in beneficial effects between the 2 drugs. DISCUSSION: Valproate and topiramate seem to be able to manage successfully chronic migraine without substantial differences in efficacy and tolerability. This affords clear practical advantages-in the event of failure of or intolerance for one treatment, the patient may be switched to the other.

Adult↗
PubMed1984

Coffee, sugars, and chronic diarrhea. Why a dietary history is important.

Patients with chronic diarrhea should be carefully questioned about their diet. A correlation may be found between gastrointestinal symptoms and the ingestion of coffee, milk, or sugars such as sorbitol and fructose. If the offending agent can be identified and withdrawn from the diet, the diarrhea will stop and further evaluation can be avoided.

Chronic Disease↗
PubMedDate not supplied

[Topiramate therapy in patients with refractory epilepsy].

AIMS: The purpose of this study was to examine the result of administrating topiramate (TPM) to patients with epilepsy that is refractory to treatment with two or more antiepileptic agents. PATIENTS AND METHODS: A total of 50 patients were evaluated, 90% of which had partial seizures (simple partial, complex partial and partial with secondary generalisation) and the remaining 10% suffered from generalised seizures. The most frequent aetiology was that which corresponded to the symptoms (52% of the cases). 98% of the patients were treated with two or three drugs. TPM was added with a dosage interval between 75 and 550 mg and follow-up visits were carried out throughout a period of nine months. RESULTS: 12 patients remained seizure-free for at least the first three months of the study; in 20 patients the number of seizures decreased by 50% or more; in 14 patients no changes were observed, and in the other four there was an increase in the number of seizures. The best results were obtained in cases of seizures with an idiopathic aetiology, while complex partial seizures offered the worst results. We also analysed the factors that might exert an influence on the different degrees of response. CONCLUSIONS: TPM was effective in all kinds of seizures. 24% of the patients became seizure free, and the total percentage of respondents rose to 64%. No patients dropped out of the study because of intolerance to the drugs.

Adolescent↗
PubMed1995

Impairment of the modulation by glucose of hepatic gluconeogenesis in the genetically obese (fa/fa) Zucker rat.

Genetically obese (fa/fa) Zucker rats show oral glucose intolerance, an alteration that has been attributed at least in part to an impaired suppression of hepatic glucose output after the ingestion of glucose. In this work, we studied the influence of different concentrations of glucose (2.5-30 mM) on gluconeogenesis from a mixture of [14C]lactate-pyruvate as well as on fructose 2,6-bisphosphate levels, pyruvate kinase activity, and flux through the reaction catalyzed by 6-phosphofructo-1-kinase, in hepatocytes isolated from fed obese (fa/fa) or lean (Fa/-) rats. In hepatocytes isolated from lean rats, incubation with increasing concentrations of glucose caused a dose-dependent inhibition of gluconeogenesis (5.02 +/- 0.54 and 1.82 +/- 0.33 mumol lactate converted to glucose/g cells.20 min in hepatocytes incubated in the presence of 2.5 and 30 mM glucose, respectively; n = 4 experiments; P < 0.01) together with a significant elevation of the fructose 2,6-bisphosphate content and a stimulation of the flux through 6-phosphofructo-1-kinase reaction. Glucose also provoked a dose-dependent activation of pyruvate kinase in the absence of changes in the cellular concentration of cAMP. In liver cells from obese animals, gluconeogenesis was not significantly modified by raising the glucose concentration in the incubation medium (1.26 +/- 0.11 and 0.83 +/- 0.14 mumol lactate converted to glucose/g cells.20 min in hepatocytes incubated with 2.5 and 30 mM glucose, respectively; n = 4 experiments; P = 0.11) despite significant increases in both fructose 2,6-bisphosphate levels and flux through the 6-phosphofructo-1-kinase reaction. In these cells, pyruvate kinase was only slightly activated by high glucose concentrations. These results indicate that, unlike fructose 2,6-bisphosphate levels and flux through the 6-phosphofructo-1-kinase reaction, hepatic gluconeogenesis is unresponsive to high glucose concentrations in genetically obese (fa/fa) rats.

Acetates↗