[Secondary intolerance to monosaccharides in a diarrheal syndrome with prolonged development. Presentation of 10 cases and review of the literature].
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Bile Acids and Salts↗
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Overnutrition in spiny mice (Acomys cahirinus): beta-cell expansion leading to rupture and overt diabetes on fat-rich diet and protective energy-wasting elevation in thyroid hormone on sucrose-rich diet.
PREVIOUS STUDIES: The investigation of diabetes propensity in spiny mice, performed in Geneva and Jerusalem colonies, is reviewed. Spiny mice live in semi-desert regions of the eastern Mediterranean countries. Those transferred to Geneva in the 1950s were maintained on a rodent diet supplemented by fat-rich seeds. They became obese, exhibited pancreatic islet hyperplasia and hypertrophy. Low insulin secretion response was characteristic of this species, despite ample pancreatic content of insulin. After a few months, diabetes with ketosis occurred, often suddenly, in association with islet cell disintegration. In Jerusalem the spiny mice were collected from their native habitat and placed on diets containing 50% sucrose or fat-rich seed diets. On a sucrose-rich diet, spiny mice developed hepatomegaly, lipogenic enzyme hyperactivity, and elevation in very low density lipoproteins as a result of metabolism of the fructose component mainly in the liver. No overt diabetes or pancreatic islet disintegration were observed, although insulin content and beta-cell hypertrophy and hyperplasia were apparent. On a fat-rich diet, spiny mice exhibited marked weight gain, adipose tissue growth and low hepatic lipogenesis. The obesity was accompanied by mild hyperglycemia and hyperinsulinemia with glucose intolerance leading to an occasional glucosuria after several months on the diet. NOVEL EXPERIMENTS: The sucrose diet induced an extrathyroidal elevation of triiodothyronine (T(3)). Serum T(3) level and hepatic T(4)-T(3) conversion were increased, while serum T(4) levels tended to decrease. The activity of the T(3)-inducible hepatic mitochondrial FAD-glycerophosphate oxidase and K(+)/Na(+)-ATPase, as well as body temperature were increased, indicating that the sucrose diet was associated with enhanced thermogenesis and energy-wasting metabolic cycling. The sucrose-rich diet might exert an adaptive thermogenesis-mediated defense mechanism, protecting against excessive weight gain and disruptive pancreatic islet lesion. After 18 months maintenance on sucrose-rich versus fat-rich diets the number of animals surviving was significantly higher on the sucrose diet whereas on the fat diet a significant number of animals succumbed to expansive islet cell disruption and diabetes.
Adipose Tissue↗
Tungstate is an effective antidiabetic agent in streptozotocin-induced diabetic rats: a long-term study.
AIMS/HYPOTHESIS: Recent studies have shown the anti diabetic effects of oral sodium tungstate treatment in several animal models of diabetes based on short-term experiments. In this study, we examined the effectiveness of long-term tungstate treatment of streptozotocin-induced-diabetic rats. METHODS: Tungstate was administered to the drinking water of rats for eight months. RESULTS: The treatment resulted in a reduction in serum glucose concentrations in diabetic rats, but no change in glycaemia was detected in healthy rats. Alterations in the hepatic glucose metabolism due to diabetes were almost completely counteracted by tungstate treatment. The partial recovery of glucokinase activity, not found in diabetic animals, normalised glycogen and glucose 6-phosphate concentrations. Tungstate treatment also restored pyruvate kinase activity and fructose 2,6-bisphosphate concentrations. In healthy rats, tungstate treatment did not modify the majority of the hepatic parameters studied. Moreover, tungstate treatment prevented diabetes-induced morphological changes in the kidney and ocular lens and also reduced mortality. Furthermore, no hypoglycaemic episodes or undesirable side effects were observed in treated diabetic or healthy rats. In addition, there is no evidence of intolerance developing after prolonged use. CONCLUSION/INTERPRETATION: Tungstate could play a helpful part in the long-term treatment of diabetes.
Aging↗
Evidence against a role of insulin in hypertension in spontaneously hypertensive rats. CS-045 does not lower blood pressure despite improvement of insulin resistance.
Hyperinsulinemia resulting from peripheral insulin resistance has been demonstrated both in spontaneously hypertensive rats (SHR) and in humans with essential hypertension. A new class of antidiabetic drugs, thiazolidinediones, which can improve insulin resistance, may be able to lower not only blood glucose levels but also blood pressure. The present study was therefore designed to clarify the proportion of SHR that are glucose intolerant and to observe the effect on blood pressure of CS-045 (troglitazone) administered at 70 mg/kg per day for 2 weeks to male SHR (n = 13). Among 67 male 8-week-old SHR, 74.6% were glucose intolerant and hyperinsulinemic. Systolic blood pressure did not correlate with plasma glucose or insulin levels before or after glucose loading. Treatment with CS-045 improved insulin resistance, as evidenced by a smaller area under the curve of plasma glucose and insulin levels in response to glucose loading. However, systolic blood pressure was not altered. When the data were reanalyzed according to the presence or absence of glucose intolerance before the treatment, blood pressure in the treated group was the same as in controls despite significant improvement in steady-state plasma glucose levels. These results suggest that hyperinsulinemia and/or insulin resistance may not be involved in the development or maintenance of hypertension in SHR, which is in contrast to models of hypertension such as obese Zucker rats or fructose-fed rats.
Animals↗
Effect of chronic uremia on fructose 2,6-bisphosphate glycolytic and gluconeogenic enzymes in rat liver.
The level of fructose 2,6-bisphosphate and the maximal activities of key gluconeogenic and glycolytic enzymes were determined in the liver of a rat model of chronic uremia and in ad libitum-fed control and pair-fed control animals. Fructose 2,6-bisphosphate was decreased in uremia and its level negatively correlated with the concentration of blood urea nitrogen. The changes in gluconeogenic enzymes in uremic rats were not different from those in the pair-fed controls. However, pyruvate kinase was decreased in uremia when compared to both controls. These studies offer a possible mechanism for the role of the liver in the carbohydrate intolerance of uremia.
Animals↗
Dietary vitamin e supplementation attenuates hypertension in Dahl salt-sensitive rats.
There is strong evidence that excess dietary salt (NaCl) is a major factor contributing to the development of hypertension. Salt-sensitive humans and rats develop hypertension even on a normal-salt diet. Salt sensitivity is associated with glucose intolerance and insulin resistance in both humans and animal models, including Dahl salt-sensitive (DSS) rats. In insulin resistance, impaired glucose metabolism leads to elevated endogenous aldehydes that bind sulfhydryl groups of membrane proteins, altering calcium channels, and increasing cytosolic free calcium ([Ca2+]i) and blood pressure. Vitamin E lowers tissue aldehyde conjugates, cytosolic [Ca2+]i, and blood pressure in spontaneously hypertensive rats and fructose-induced hypertensive Wistar Kyoto rats, models of insulin resistance. This study investigated the effect of a normal-salt diet on tissue aldehyde conjugates, cytosolic [Ca2+]i, and blood pressure in DSS rats and the effect of vitamin E supplementation on blood pressure and associated biochemical changes in these animals. Seven-week-old DSS rats were divided into 3 groups of 6 animals each and treated for 6 weeks with diets as follows: low-salt (0.4% NaCl); normal-salt (0.7% NaCl) and normal salt (0.7% NaCl) plus vitamin E (34 mg/kg feed). At completion, animals in the normal-salt group had significantly elevated systolic blood pressure, cytosolic [Ca2+]i, and tissue aldehyde conjugates compared with the low-salt group. They also showed smooth muscle cell hyperplasia in small arteries and arterioles of the kidney. Dietary vitamin E supplementation significantly attenuated the increase in systolic blood pressure and associated biochemical and histopathologic changes.
Aldehydes↗
Topiramate for patients with refractory migraine: an observational, multicenter study in Spain.
INTRODUCTION: The efficacy of current preventive migraine treatments is limited. In addition, tolerability problems are not infrequent. OBJECTIVES: To check our experience with topiramate in the treatment of patients with refractory migraine. PATIENTS AND METHODS: We offered treatment with topiramate to patients with the diagnosis of International Headache Society (IHS) migraine who had not responded to or tolerated beta-blockers, amitriptyline, flunarizine and/or valproate. This series is made up of 115 patients (88 women), between 16 and 81 years. Most of them (n=79) fulfilled the Silberstein et al. criteria for transformed migraine. The parameters analyzed were "response" (reduction in migraine frequency>50%), excellent response (>75%) and tolerability. RESULTS: After 3 months, the maintenance doses of topiramate ranged from 25 to 400 mg, though most patients took 100 mg. Twenty-four (21%) patients withdrew due to adverse events, mostly cognitive difficulties, that had already occurred with doses as low as 25-50 mg, while 26 (23%) found topiramate ineffective. The remaining 65 (56%) patients responded, 34 with excellent response. Sixteen patients (10 obese) lost weight (3-13 kg). CONCLUSIONS: Topiramate seems to be a good therapeutic option for about half of the patients with refractory migraine. In these patients response is usually excellent. Intolerance due to adverse events appears in one-fifth of the cases early and at low doses.
Adolescent↗
Aldosterone stimulates gene expression of hepatic gluconeogenic enzymes through the glucocorticoid receptor in a manner independent of the protein kinase B cascade.
Primary aldosteronism is associated with glucose intolerance and diabetes, which is due in part to impaired insulin release caused by reduction of potassium, although other possibilities remain to be elucidated. To evaluate the in vivo effects of aldosterone on glucose metabolism, a single dose of aldosterone was administered to mice, which resulted in elevation of the blood glucose level. In primary cultured mouse hepatocytes, the gene expression of gluconeogenic enzymes such as glucose-6-phosphatase (G6Pase), fructose-1,6-bisphosphatase and phosphoenolpyruvate carboxykinase increased in response to aldosterone in a dose-dependent manner even at a concentration similar to a physiological condition (10(-9) M). The inhibitory effect of insulin on G6Pase gene expression was partially suppressed by aldosterone. Furthermore, aldosterone enhanced G6Pase promoter activity in human hepatoma cell line HepG2, which was prevented by co-treatment with a glucocorticoid antagonist RU-486, but not a mineralocorticoid antagonist spironolactone. In contrast, aldosterone had no effects on major insulin signaling pathways including insulin receptor substrate-1, protein kinase B, and forkhead transcription factor. These results suggest that aldosterone may affect the inhibitory effect of insulin on hepatic gluconeogenesis through the glucocorticoid receptor, which may be one of the causes of impaired glucose metabolism in primary aldosteronism.
Aldosterone↗
Treatment of cluster headache with topiramate: effects and side-effects in five patients.
We report on clinical experience with topiramate in the prophylactic treatment of three patients with chronic and two patients with episodic, otherwise therapy-resistant, cluster headache. Patients were treated with daily doses of 75-200 mg topiramate. Topiramate was effective in three patients but proved ineffective and also caused intolerable side-effects in two patients. Topiramate may have prophylactic properties for treating cluster headache at lower doses than needed in epilepsy therapy, but its clinical value is limited due to central nervous system side-effects.
Adult↗
Topiramate after adjustable gastric banding in patients with binge eating and difficulty losing weight.
BACKGROUND: About 15% of patients who undergo adjustable gastric banding (AGB) have difficulty losing weight due to, among other factors, the development or maintenance of binge eating disorder. Topiramate is an anticonvulsive drug with proven good results in controlling binge eating episodes. The objective of this study was to analyze the effect of topiramate in patients with AGB. METHODS: 16 patients with binge eating and inadequate weight loss after AGB were analyzed prospectively for 3 months while receiving topiramate in doses varying from 12.5 to 50 mg per day. RESULTS: There was a mean increase in excess weight loss from 20.4% to 34.1% without the need for band readjustment. 2 patients had intolerance to topiramate and were changed to fluoxetine 40 mg per day. CONCLUSION: Topiramate may be a useful adjuvant for patients with AGB and binge eating disorder.
Adolescent↗
Genetic and biochemical analysis of anaerobically-induced enzymes during seed germination of Echinochloa crus-galli varieties tolerant and intolerant of anoxia.
To compare the regulation of anaerobic metabolism during germination in anoxia-tolerant and intolerant plants, enzymes associated with anaerobic metabolism such as sucrose synthase, aldolase, enolase, pyruvate decarboxylase (PDC), alcohol dehydrogenase (ADH), and aldehyde dehydrogenase (ALDH) were assayed in two varieties of Echinochloa crus-galli, formosensis (tolerant) and praticola (intolerant). The initial and intervening enzymes of the pathway (sucrose synthase and aldolase) and enzymes in the last part of the pathway (PDC, ADH and ALDH) revealed similar changing patterns in activities during germination. This implies that each group of enzymes may be controlled by an identical regulatory mechanism. During anoxia, activities of all enzymes increased 1.5-30-fold in both varieties compared to their activities under aerobic conditions. Activities of sucrose synthase, enolase and ADH exhibited the same induction patterns under anoxia in formosensis and praticola. However, the activities of aldolase, ALDH and PDC were more strongly induced in formosensis under anoxia (1.2-2-fold) than in praticola. These enzymes were also assayed in F(3) families which varied in their anaerobic germinability. For PDC, activities under anoxia in anoxia-tolerant families were similar to those of an anoxia-intolerant family during the whole period although the family did not exhibit anaerobic germinability. This suggests that there is no correlation between PDC activity and anaerobic germinability. For ALDH, activities were more strongly induced under anoxia in anoxia-tolerant families than in anoxia-intolerant families, a trend also exhibited by the parents. This indicates that ALDH may play a role in detoxifying acetaldehyde formed through alcoholic fermentation during anaerobic germination.
Adaptation, Physiological↗
Hypertriglyceridemia and carbohydrate intolerance: interrelations and therapeutic implications.
Atherosclerosis, the most frequent complication of diabetes, could be the result of hyperlipidemia, among other factors. Mounting evidence suggests that reducing the concentration of triglyceride-rich lipoprotein, which influences the production of the possibly atherogenic intermediate density lipoprotein (IDL), might diminish the circulating level of potentially atherogenic lipoproteins. Hypertriglyceridemia, even in the absence of obesity, is associated with insulin resistance. To compensate, pancreatic B cells respond to glucose challenge by producing hyperinsulinemia. If the B cells cannot respond adequately, carbohydrate intolerance ensues. Insulin-treated diabetics may also become hyperinsulinemic because routine insulin injection may not reflect physiologic need and because the insulin is administered peripherally rather than portally. Hyperinsulinemia increases the production of circulating triglyceride. It appears to do this in rats by causing the production of more triglyceride-rich lipoprotein particles rather than by increasing the triglyceride content of each particle. Further, at least in rats, the insulin-induced increase in triglyceride production requires the presence of supplementary dietary fructose. Hyperinsulinemia also increases the activity of adipose tissue lipoprotein lipase and the degradation of very low density lipoprotein (VLDL). The concentration of VLDL depends on balance of production and degradation. Accelerated VLDL degradation leads to an increase in IDL production. Because there is mounting evidence that IDL may be atherogenic, this cycle could accelerate atherogenesis. As such, it is reasonable to postulate that reducing the concentration of triglyceride-rich lipoproteins would break this cycle and would diminish the circulating level of potentially atherogenic lipoproteins.
Arteriosclerosis↗
Abnormalities of carbohydrate metabolism in idiopathic Fanconi syndrome.
Various metabolic studies were performed in a patient with the idiopathic Fanconi syndrome in whom constant ketonuria suggested that organic acidemia might contribute to the metabolic acidosis. Glucose intolerance with a diminished insulin release was found after PO or IV glucose loads and after glucagon administratio. An insulinopenic "diabetes-like" state has not previously been described in such patients. The patient had impaired galactose-glucose interconversion, elevated blood lactate levels, reduced pyruvate levels, and an increased lactate:pyruvate ratio. Hepatomegaly and hypoglycemia were not present, and liver and muscle biopsies revealed no enzymatic evidence of glycogenosis. The erythrocyte UDP galactose transferase activity was normal. The patient failed to convert fructose to glucose and had a rise in blood lactate after ethanol administration. Further studies revealed no production of glucose after alanine or glycerol administraion, each test being associated with elevated blood lactate levels and, after alanine, an increased lactate:pyruvate ratio. The lactate:pyruvate ratio was elevated after glucagon administration with increased lactate and reduced pyruvate concentrations.
Carbohydrate Metabolism↗
[Association between dietary carbohydrates and type 2 diabetes mellitus: epidemiological evidence].
The prevalence of type 2 diabetes has been escalating throughout the world and usual food consumption is regarded as one of the most important environmental determinants for chronic diseases. Thus, the role of type and quality of carbohydrates on the etiology of type 2 diabetes is still poorly understood. The present review discusses the available epidemiological evidence regarding the effect of the type and source of carbohydrate of the usual diet and the risk of type 2 diabetes in adults. Although epidemiological investigations support the hypothesis for a potential risk effect of high glycemic index and low fiber content diets for diabetes, the results are controversial and the benefit may be related to the magnesium content of the structure of the grains, suggesting the relevance of taking into account the food sources instead of nutrients on investigations of diet and risk of chronic diseases. The available evidence suggests that eating a diet rich in whole grain cereals and vegetables and low in refined grains, sucrose and fructose contents is beneficial in the prevention of diabetes. Thus, more clinical trials are required to support the associations and establish biologically plausible pathways.
Adult↗
[Carbohydrate intolerance during complete fasting].
In the first part of the study oral glucose tolerance tests (GTT) or insulin tolerance tests (ITT) were performed in 22 lean and 22 obese nondiabetics before and after fasts of at least 6 days' duration. Deterioration of glucose tolerance was greater in lean than in obese individuals. Plasma levels of factors known to influence glucose tolerance (glucagon, growth hormone, free fatty acids, ketones) were significantly higher in fasting lean than in fasting obese subjects. Furthermore, delayed insulin rise (GTT) and decreased insulin sensitivity (ITT) were observed after starvation in lean subjects but not in the obese, which could explain the greater deterioration of glucose tolerance in the lean population. In the second part of the study glucose and fructose tolerance were compared during 4-hour infusions of these substrates (0.5 g/kg/h) in 8 normal subjects before and after two 4-day fasts. After starvation, glucose as well as fructose infusion resulted in plasma levels of the infused hexose significantly higher than in control, and the rise in plasma lactate and pyruvate was delayed. These results contradict the view widely held in the literature, that fructose metabolism remains unimpaired in the fasting state.
Adult↗
Visceral factors in the control of food intake.
Some years ago, we reported that the increased blood intake of hypoglycemic rats was inhibited by the intravenous infusion of fructose, a sugar that cannot cross the blood-brain barrier and nourish cerebral chemoreceptors. More recent experiments therefore have focused on visceral factors in the control of food intake. Three observations have been emphasized in this review. First, we found that gastric emptying was increased during insulin-induced hypoglycemia, and that this effect also was eliminated by administration of fructose. Hepatic vagotomy abolished both this effect of fructose on gastric emptying and its effect on food intake. Second, we found that in rats with severe diabetes, the rate of gastric emptying did decrease in proportion to increasing concentration of an administered glucose load, as it does in intact rats, but calories emptied more rapidly than normal regardless of the concentration of the load. Third, we found that rats with varying degrees of streptozotocin-induced damage to the pancreas ate more food than intact rats did after an overnight fast, and that individual intakes were proportional to the induced glucose intolerance. The increased eating took the form of shorter intermeal intervals, as if the initial postfast meal did not remain satiating for a normal amount of time. These and other findings suggest that food intake is controlled in part by satiety signals apparently related to the delivery of utilizable calories plus insulin to the liver. These signals also seem to affect gastric emptying and thereby might influence other satiety signals related to gastric distention.
Animals↗
Alpha 2-adrenergic agonists increase cellular lactate efflux.
We reported previously that genetic polymorphisms of the alpha 2-adrenergic receptor are associated with hyperinsulinemia, diabetes mellitus, and hypertension in blacks. The evolutionary driving force for maintaining such deleterious mutations in the black population is unknown. Recognizing that vascular alpha 2-adrenergic receptors mediate cold-induced vasoconstriction and that temperature maintenance is a primary thrust of cellular metabolism, we postulated that vascular alpha 2-adrenergic receptors contribute significantly to metabolic heat generation in homeotherms such as humans. Using aerobic lactate production as an indicator of thermogenesis, we measured metabolic heat production in HT29 cells that expressed the gene encoding human vascular alpha 2-adrenergic receptors. Epinephrine, an alpha 2-adrenergic receptor agonist, increased net lactate efflux from 226 +/- 20 to 280 +/- 20 nmol/min (mean +/- SE) (P = .06). Clonidine, a more specific alpha 2-adrenergic agonist, increased lactate efflux from 110 +/- 6 to 156 +/- 8 nmol/min (P < .01). Similarly, in the presence of physiological concentrations of glucose (5.5 mmol/L), insulin increased lactate production from 123 +/- 6 to 175 +/- 10 nmol/min (P < .01). Because differences in aerobic glycolysis may also explain the heat intolerance and abnormal fuel homeostasis found in genetically hypertensive rats, we also measured lactate production in cultured vascular smooth muscle cells isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive control Wistar-Kyoto rats (WKY). Vascular smooth muscle cells from SHRSP had significantly greater lactate efflux compared with cells from normotensive WKY (296 +/- 4 versus 172 +/- 2 nmol/min, P < .001). These differences were not due to abnormalities in glucose uptake, as lactate efflux was greater in SHRSP cells compared with WKY cells when dextrose was replaced with equimolar concentrations of fructose (230 +/- 6 versus 138 +/- 2 nmol/min, P < .001). alpha 2-Adrenergic agonists increase lactate efflux in HT29 cells, and abnormalities in vascular smooth muscle lactate metabolism in genetically hypertensive rats is independent of altered glucose uptake. These data provide support for our hypothesis that balanced polymorphisms of the alpha 2-adrenergic receptor could offer protection against cold stress by increasing the thermogenic response associated with aerobic lactate production.
Adrenergic alpha-Agonists↗
Topiramate in the treatment of severe bulimia nervosa with comorbid mood disorders: a case series.
OBJECTIVE: To report observations on the efficacy and tolerability of topiramate in a sample of five patients with severe symptoms of bulimia nervosa and comorbid mood and/or anxiety disorders. METHOD: Topiramate was added to other psychotropic medication under open-label conditions up to the maximum tolerated dose or until remission of the eating disorder was achieved. RESULTS: Topiramate almost completely eliminated binging and purging behavior in three of the five patients. Improvement was maintained throughout the period of follow-up for up to 18 months. One patient showed a partial, temporary response, and the fifth was intolerant of the drug and unable to complete an adequate trial. DISCUSSION: These results suggest strongly that the efficacy of topiramate in patients with bulimia nervosa with and without comorbid mood and anxiety disorders should be investigated more fully.
Adult↗