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PubMed2000

[Insulin sensitizer and hypertension].

Insulin resistance syndrome is the theory that glucose intolerance, hyperinsulinemia, increased very low density lipoprotein triglyceride level, decreased high density lipoprotein cholesterol level, and hypertension are proposed consequences of insulin resistance. In this theory, insulin resistance and the resultant hyperinsulinemia are considered to raise blood pressure through 1) sympathetic nervous system activation, 2) renal sodium retention, 3) renin-angiotensin system stimulation, and 4) intracellular calcium accumulation in vascular smooth muscle. Indeed, metabolic disturbance and insulin resistance have been pointed out in essential hypertensives. The effect of insulin sensitizer on blood pressure have been investigated in human and animal experiments. It has been clarified that troglitazone reduces blood pressure in essential hypertensives and fructose fed rats. However, it has also been reported that troglitazone did not lower blood pressure in SHR and fructose fed rats. Further study will be necessary to clarify the effects of insulin sensitizer on blood pressure.

Animals↗
PubMed2002

Physiological small bowel malabsorption of carbohydrates protects against large bowel diseases in Africans.

In African black people there is a paucity of 'developed society' large bowel diseases such as diverticular disease, colorectal adenomas and carcinomas, ulcerative colitis and Crohn's disease. Appendicitis has an incidence of about 5-10% of the number likely to be observed in a white population. The conundrum is that the disparity exists despite many Africans having adopted an urbanized lifestyle with major changes in their dietary pattern. Dietary fiber intake, which was previously 30-35 g, has decreased to 12-14 g daily. Studies on small bowel function in black people have shown that physiological malabsorption of lactose, fructose, sucrose and maize (the staple food) occurs. It is hypothesized that the increased concentration of substrate available for fermentation in the colon compensates for the low dietary fiber intake, is protective to the large bowel and is a factor in the prevention of 'developed society' large bowel diseases in the African population.

Asian People↗
PubMed2003

Painful diabetic peripheral neuropathy relieved with use of oral topiramate.

Diabetic peripheral neuropathy affects 5 to 50% of people with diabetes in the United States. It is a progressive disorder that results in a gradual decrease in peripheral sensation and eventually complete loss of sensation. Patients with diabetic peripheral neuropathy are challenging to treat because of intolerable adverse medication effects and the development of tolerance to medical treatment. We present the case of a patient with peripheral neuropathy that was unresponsive to usual therapies. She experienced significant relief with the administration of topiramate. Topiramate is an anticonvulsant that is gaining recognition in the treatment of patients with neuropathic pain syndromes.

Administration, Oral↗
PubMed1979

The effect of aging on carbohydrate metabolism: a review of the English literature and a practical approach to the diagnosis of diabetes mellitus in the elderly.

There seems little doubt that the disposal of a glucose load is progressively impaired during aging. The mechanism(s) for this alteration remains unclear. Five possibilities have been raised: (1) poor diet, (2) physical inactivity, (3) decreased lean body mass in which to store the carbohydrate load, (4) decreased insulin secretion, and (5) insulin antagonism. Although poor diet and physical inactivity may contribute to some of the abnormal glucose tolerance tests of the older population, these two factors do not provide a full explanation. Diminished lean body mass may play some role but there is almost certainly an additional effect due to aging. A few papers have suggested that glucose-induced insulin secretion may be impaired as the population ages, but the bulk of studies in this area conclude that normal or increased amounts of insulin are released by the pancreatic beta-cell during aging. If abnormalities of insulin secretion exist, either in degree or timing, they are subtle and would not seem sufficient to account for the great number of older subjects who manifest impaired glucose tolerance. The evidence for insulin antagonism seems the strongest but the data are certainly not conclusive. In actuality, the aging effect on carbohydrate metabolism may be heterogeneous in nature. Either some or all of these five factors may contribute to the aging effect to varying degrees in individual subjects. Alternatively, the glucose intolerance of aging may represent a heterogeneous group of disorders. In any event, until better methods to identify possible subgroups of these subjects and/or a marker for diabetes mellitus independent of glucose concentration become available, this problem will remain difficult to resolve. Based on the currently available data, it seems prudent to diagnose diabetes mellitus only if fasting hyperglycemia is present.

Aged↗
PubMed1997

Effects of energy limitation on Ca2+ and K+ homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes.

To gain more insight into the mechanistic basis of anoxia tolerance and intolerance, a comparative study was conducted on calcium homeostasis in goldfish and trout hepatocytes subjected to different forms of energy limitation. Using the fluorescent Ca2+ indicator fura 2, we observed that both chemical anoxia and true anoxia led to an increase of the concentration of cytosolic free calcium (Ca2+i) in the anoxia-sensitive hepatocytes of rainbow trout, whereas Ca2+i was maintained at control levels in the anoxia-tolerant hepatocytes of goldfish. Various lines of evidence suggest an intracellular origin of the Ca2+ increase observed in trout cells. Cyclosporin A, a specific inhibitor of the mitochondrial permeability transition pore in mammalian cells, was ineffective in preventing the Ca2+ increase, whereas a high dose of fructose depressed the Ca2+ surge by approximately 50%. The latter effect was not accompanied by improvement of the energetic state of the cells. A comparison of chemical anoxia with true (physiological) anoxia revealed that both treatments affected energy metabolism to a similar degree in trout hepatocytes, whereas the decrease of ATP seen in goldfish hepatocytes during chemical anoxia was absent during true anoxia. Elevation of Ca2+i with the calcium ionophore A-23187 led to a decoupling of unidirectional K+ fluxes in both normoxic and anoxic trout cells, whereas in goldfish hepatocytes the coupling of K+ fluxes was not affected by the rise of Ca2+i.

Adenosine Triphosphate↗
PubMed1999

Topiramate in clinical practice: first year's postlicensing experience in a specialist epilepsy clinic.

OBJECTIVE: Topiramate became available for use in October 1995. Meta-analysis of its randomised controlled data suggested that it may be the most potent of the new antiepileptic drugs. The aim of this study was to assess the first year's postlicensing experience in a specialist regional epilepsy clinic. METHODS: The case notes of 174 of 178 patients who were prescribed topiramate in the 12 months between November 1995 and October 1996 were retrospectively reviewed. Data were collected on seizure type, classification of epilepsy, presence or absence of learning difficulties, depression, or behavioural problems, co-medication, dosage escalation, efficacy, adverse events, whether or not the patient was still on topiramate and, if not, the reason for withdrawal. Kaplan-Meier survival analysis was used to estimate the overall retention rate and log rank tests were used to determine factors associated with stopping topiramate. RESULTS: Overall 90 of 174 patients had ceased taking topiramate at the end of the study. The median "survival time" was 427 days (95% CI 362.9-491.1). The cumulative probability for remaining on topiramate at 1 year was 0.549 (95% CI 0.475-0.623). The retention rate in patients in whom topiramate was substituted for another drug was significantly higher than in those in whom it was added to current therapy. Adverse events (CNS related) were the most common reason for stopping topiramate. Eight patients with partial and one patient with juvenile myoclonic epilepsy became seizure free. CONCLUSIONS: There is a significant (20-25%) chance of being intolerant to topiramate at relatively low doses. Substituting topiramate for another antiepileptic drug may reduce the chances of drug withdrawal. If topiramate is tolerated there is a good chance of worthwhile improvement in seizure control. These data, although not derived from randomised controlled trials, represent pragmatic use of novel antiepileptic drugs in "real life" and may be helpful to non-specialists when prescribing topiramate.

Anticonvulsants↗
PubMed2002

Role of topiramate in adults with intractable epilepsy, mental retardation, and developmental disabilities.

The efficacy and safety of topiramate in patients with intractable mixed seizures, mental retardation (MR), and developmental disabilities (DD) were investigated. Twenty patients (eight females and 12 males) aged 21-57 years old with intractable epilepsy with mixed seizures, MR [profound (five), severe (three), moderate (two), mild (eight) and borderline (two)], and DD were treated with adjunctive topiramate 25 mg per day for 1 week followed by titration to clinical response (range 50-350 mg per day). Other antiepileptic drugs (AEDs) were decreased simultaneously. Topiramate therapy was discontinued in four patients for adverse events consisting of disorientation, unsteadiness, and pneumonia (one patient); anaphylactic shock from a tuna fish allergy (one); patient choice (one); and loss to follow-up (one). Seizures improved by gt-or-equal, slanted 50% in 11 of 16 patients (69%). Two patients (13%) were seizure free, including one patient who prior to topiramate therapy was seizure free but experiencing an intolerable adverse effect during therapy with another AED. Seizure duration and/or severity decreased in seven patients (44%). An increase in alertness was observed in 11 patients (59%). Topiramate was associated with improvement in seizure severity and alertness in this series and may be useful as adjunctive therapy in patients with mixed seizures, MR, and DD.

Adult↗
PubMed1999

Topiramate in intractable childhood onset epilepsy--a cautionary note.

OBJECTIVES: To study the effectiveness and safety of topiramate in clinical practice, for a group of patients with childhood onset epilepsy. METHODS: All patients treated with topiramate at the three study centers between November 1995 and December 31, 1997 were analyzed retrospectively, using a standardized study protocol. Data were gathered on demographic features, seizures response and medication related adverse events. RESULTS: Eighty-seven patients were treated with topiramate. Over 90% seizure reduction was achieved in 8 (9%) patients, 50%-90% in 21 (24%), < 50% in 54 (62%) patients. Four patients (5%) had a deterioration in seizure control. Adverse events required topiramate discontinuation in 36 (41%). Of these 27 (31%) complained of unacceptable cognitive dulling. The rate of dose escalation and final dose in mg/kg were similar in those who remained on topiramate and those who were intolerant because of cognitive side effects. CONCLUSIONS: Although topiramate resulted in > 50% seizure reduction in 29 (33%) of this group of patients with difficult epilepsy, its usefulness was limited by a high incidence of adverse effects. Adverse events prevented ongoing therapy for 36 (41%) and cognitive dulling resulted in topiramate discontinuation by 27 (31%) of the group.

Adolescent↗
PubMed2004

Emerging experimental therapeutics for bipolar disorder: insights from the molecular and cellular actions of current mood stabilizers.

Bipolar disorder afflicts approximately 1-3% of both men and women, and is coincident with major economic, societal, medical, and interpersonal consequences. Current mediations used for its treatment are associated with variable rates of efficacy and often intolerable side effects. While preclinical and clinical knowledge in the neurosciences has expanded at a tremendous rate, recent years have seen no major breakthroughs in the development of novel types of treatment for bipolar disorder. We review here approaches to develop novel treatments specifically for bipolar disorder. Deliberate (ie not by serendipity) treatments may come from one of two general mechanisms: (1) Understanding the mechanism of action of current medications and thereafter designing novel drugs that mimics these mechanism(s); (2) Basing medication development upon the hypothetical or proven underlying pathophysiology of bipolar disorder. In this review, we focus upon the first approach. Molecular and cellular targets of current mood stabilizers include lithium inhibitable enzymes where lithium competes for a magnesium binding site (inositol monophosphatase, inositol polyphosphate 1-phosphatase, glycogen synthase kinase-3 (GSK-3), fructose 1,6-bisphosphatase, bisphosphate nucleotidase, phosphoglucomutase), valproate inhibitable enzymes (succinate semialdehyde dehydrogenase, succinate semialdehyde reductase, histone deacetylase), targets of carbamazepine (sodium channels, adenosine receptors, adenylate cyclase), and signaling pathways regulated by multiple drugs of different classes (phosphoinositol/protein kinase C, cyclic AMP, arachidonic acid, neurotrophic pathways). While the task of developing novel medications for bipolar disorder is truly daunting, we are hopeful that understanding the mechanism of action of current mood stabilizers will ultimately lead clinical trials with more specific medications and thus better treatments those who suffer from this devastating illness.

Antimanic Agents↗
PubMed2003

Transgenic expression of CD36 in the spontaneously hypertensive rat is associated with amelioration of metabolic disturbances but has no effect on hypertension.

Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1 alpha promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure.

Adipose Tissue↗
PubMed2004

Chronic hypoxia: common traits between chronic obstructive pulmonary disease and altitude.

PURPOSE OF REVIEW: Loss of body mass and exercise intolerance are common findings in chronic obstructive pulmonary disease and are often difficult to reverse despite optimal nutritional intake. Similar findings have been reported in healthy individuals during high-altitude exposure. The role of hypoxia in modulating metabolism has been largely investigated in vitro and in animal studies. More fragmentary is the knowledge regarding hypoxia effects on in-vivo human metabolism. This paper reviews recent literature regarding the effects of chronic exposure to hypoxia on metabolism, particularly comparing chronic obstructive pulmonary disease patients with humans exposed to high altitude. RECENT FINDINGS: Hypoxia has important metabolic effects. Many oxygen-sensitive regulatory mechanisms work through hypoxia inducible factor 1, and recent literature regarding the hypoxic stimulus and its pathological implications deals largely with hypoxia inducible factor 1-related findings. Hypoxia inducible factor 1 is pivotal in the adaptation to chronic hypoxia: it induces gene expression for fructose-2-6-biphosphatase, an enzyme switching glucose metabolism towards glycolysis, allowing energy production in anaerobic conditions. Hypoxia inducible factor 1 is also involved in the development of anorexia because it induces the promoter of the leptin gene. Particularly important for future therapeutic implications are findings related to hypoxia inducible factor 1 polymorphism and interaction with other molecules, especially estrogens, in the clinical evolution of disease. SUMMARY: Malnutrition is a worsening factor in chronic obstructive pulmonary disease. Similarities between chronic obstructive pulmonary disease and altitude exposure point to the importance of hypoxia in this regard. A better understanding of the underlying mechanisms will help to find alternative therapeutic approaches.

Altitude↗
PubMed1998

Advances in the medical treatment of epilepsy.

Treatment options for epilepsy, especially using antiepileptic drugs, have increased substantially in the past five years. Since 1993, four novel antiepileptic drugs have been approved and marketed in the United States: felbamate, gabapentin, lamotrigine, and topiramate. Two others, tiagabine and vigabatrin, are likely to be approved in the near future. For many patients, these agents offer the realistic promise of improved seizure control, often with fewer adverse effects and less significant drug interactions compared with older agents. In addition, fosphenytoin, a water-soluble phenytoin prodrug with a number of advantages over intravenous phenytoin, has been released. There are new administration options for carbamazepine, diazepam, and valproic acid. For drug-resistant or -intolerant patients, there has been renewed interest in alternative therapies, especially the ketogenic diet. Taken together, these represent significant therapeutic advances that are benefiting patients with epilepsy. At the same time, improved understanding of the basic mechanisms of epileptogenesis, and of the cellular and molecular actions of available antiepileptic drugs, creates a framework for designing unique therapeutic strategies that are targeted at key sites of vulnerability involved in the development and maintenance of the epileptic state.

Acetates↗
PubMed1987

Blood glucose and plasma insulin responses to fat free milk and low-lactose fat free milk in healthy human volunteers.

The blood glucose and plasma insulin responses to test milk samples were studied in healthy normal volunteers. After an overnight fast the subjects were given 500 ml of either regular fat free milk (approximately 25 g lactose) or 500 ml of a new low-lactose fat free milk (3.75 g lactose and 4.25 g fructose). Blood glucose levels were not significantly altered after either milk sample, but plasma insulin responses were significantly elevated after milk consumption. The response was slightly but not significantly higher after regular fat-free milk than after the low-lactose fat free milk. The results suggest that fat free milk does not exert a fast effect on blood glucose concentration and therefore fat free milk and especially low-lactose fat free milk may prove to be suitable for diabetic diets.

Animals↗
PubMed1975

Intrinsic asthma associated with diabetes mellitus; abnormal vascular response and glucose tolerance tests.

Patients manifesting intrinsic idiopathic rhinitis and/or asthma in association with diabetes or aspirin intolerance were studied. Various metabolites (sugars and L-histidine) and chemical (aspirin, insulin and glucagon) challenges were studied using the parameter of the induced sequential vascular response. A standard oral glucose tolerance test was also correlated. The results indicated similar as well as divergent ab- nc. nalities of responses to the various carbohydrates, insulin, glucagon, L-histidine and aspirin challenges. This permitted a separation of some patients with idiopathic rhinitis and/or asthma into those associated with diabetes and those with tolerance to aspirin.

Aspirin↗
PubMed2005

Levetiracetam for mood stabilization and maintenance of seizure control following multiple treatment failures.

OBJECTIVE: To report the case of a patient who experienced adverse events in succession to antiepileptic medications being used for both antiepileptic and mood-stabilization benefit. CASE SUMMARY: A 46-year-old white woman developed hyponatremia with carbamazepine, hyperammonemia with divalproex, cognitive impairment with topiramate, and hyponatremia with oxcarbazepine. The patient was stabilized physically and psychiatrically on levetiracetam without any noted adverse events. DISCUSSION: The adverse events in this report have been associated with the medications in question. The patient's presentation is unique, as she developed adverse events in succession to antiepileptic drugs being used to treat both a seizure disorder and symptoms of mood instability. The Naranjo rankings for the reported adverse events indicated the associations were probable (carbamazepine, divalproex, oxcarbazepine) and possible (topiramate). After repeated incidences of intolerability to these drugs, levetiracetam was initiated and provided both seizure control and mood-stabilizing benefits, which eventually led to hospital discharge. CONCLUSIONS: Levetiracetam may provide mood-stabilizing qualities through a mechanism that is unique from that of other antiepileptic agents used for their mood-stabilizing properties. There are potential advantages with levetiracetam, as no specific therapeutic drug monitoring parameters need to be followed after its introduction. Additionally, this case emphasizes the importance of therapeutic drug monitoring and frequent assessments to prevent physical and psychiatric adverse reactions.

Anticonvulsants↗
PubMed2003

Oligohydrosis and hyperthermia: pilot study of a novel topiramate adverse effect.

A 6-year-old boy with partial complex seizures developed recurrent episodes of hyperthermia 2 months after topiramate was introduced into his antiepilepsy drug regimen. Further investigation revealed that the febrile episodes were related to environmental temperature and physical activity. A pilocarpine iontophoresis sweat test showed that the amount of sweat produced by the child was 5% that of age-matched controls. Topiramate discontinuation resulted in the disappearance of febrile episodes and normalization of sweat quantity in repeat sweat testing. Based on this observation and the previous data on zonisamide and isolated case reports on topiramate-related hyperthermia and the effect on sweat production, topiramate was suspected of causing oligohydrosis. A pilot study was carried out involving 13 additional children and young adults (age range 1-37 years) receiving topiramate. All patients were directly questioned regarding symptoms of decreased sweating and heat intolerance, went through a pilocarpine iontophoresis sweat test, and were compared with 14 age-matched controls who went through the sweat test for unrelated reasons. Nine of the patients were found to have reduced sweat quantity on the pilocarpine iontophoresis sweat test (including index case) (mean 0.089 g/30 minutes, SD 0.082; age-matched control: mean 0.21 g/30 minutes, SD 0.06). Eight of them were children (below 16 years). However, only three patients revealed symptoms related to heat intolerance. Topiramate is most likely responsible for decreased sweat production as detected by a pilocarpine iontophoresis sweat test. The effect seems to be more significant in children than in adults. There is a discrepancy between test results and clinical symptoms. Interestingly, oligohydrosis was found to be a relatively common side effect of zonisamide. Both zonisamide and topiramate share a carbonic anhydrase inhibitor activity. The significance of oligohydrosis in hot climates should not be underestimated. Its extent, the role of sweat test prediction, and clinical significance during topiramate treatment should be further estimated.

Adolescent↗
PubMed1981

Metabolic abnormalities in the idiopathic Fanconi syndrome: studies of carbohydrate metabolism in two patients.

Two patients with idiopathic Fanconi syndrome and glucose intolerance were studied from a metabolic perspective. They had fasting hyperglycemia, massive glucosuria, insulinopenia, ketosis, and elevated serum free fatty acids. There was a markedly blunted insulin secretory response to glucagon, tolbutamide, glucose, and arginine. One patient had the findings of diabetic retinopathy and a sensory neuropathy. Neither patient could convert galactose to glucose, but they did not have galactosemia. As a result of these studies, and previous reports in which similar changes were noted, we conclude that diabetes mellitus may occur in patients who have had idiopathic Fanconi syndrome for many years.

Adolescent↗
PubMed1988

Banting lecture 1988. Role of insulin resistance in human disease.

Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)

Coronary Disease↗