Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “hypoglycemic”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 775 records · Page 43Linked to original sources
PubMed1990

Topical application of the hypoglycemic agent glibenclamide and changes in blood glucose, plasma insulin (IRI) levels and plasma concentration of glibenclamide in normal rats.

This study was done to determine whether an oral hypoglycemic agent would be absorbed through the skin and consequently lower blood glucose levels. We applied 250 mg or 500 mg of 5% glibenclamide ointment (GO) to the cleanly shaved dorsa (5 x 10 cm) of overnight-fasted male Wistar rats, weighing 250-300 g. Blood samples were collected at 1, 3, 6, 12 and 24 h after the application of GO and blood glucose, plasma insulin (IRI) and the plasma concentration of glibenclamide were determined. The plasma concentration of glibenclamide reached a high level as early as 1 h after application and the level was maintained for 24 h. The plasma concentration of glibenclamide in the 500-mg GO group was higher than in the 250-mg GO group, but even 24 h after application the 250-mg GO group showed a mean value of 206 ng/ml. Mean blood glucose levels in both GO groups at every time point after application were significantly lower than in the control group; with respect to mean IRI levels the opposite was found. Thus, glibenclamide is absorbed through the skin and reaches a level of plasma concentration which induces significant changes in blood glucose and IRI levels. This may well be a new approach to controlling blood glucose levels in patients with diabetes mellitus.

Administration, Topical↗
PubMedDate not supplied

Evaluation of hypoglycemic counterregulation using a modification of the Andres glucose clamp.

The glucose clamp, developed by Andres for the quantification of insulin action and secretion, was modified to study counterregulatory mechanisms against hypoglycemia, thereby overcoming the technical difficulties in producing a standardized, reproducible hypoglycemic stimulus. Normal subjects are exquisitely sensitive to small decrements in glucose; levels within the normal range cause suppression of endogenous insulin (approximately 4.0 mM) and activation of glucagon and epinephrine (approximately 3.5 mM) secretion. The glucose threshold for hormone release is modified by multiple factors, including age, gender, and the level of insulin per se. If glucose continues to fall toward 3.0 mM, the hormonal response is intensified and symptoms appear. The window between the appearance of symptoms triggering carbohydrate ingestion and the earliest signs of neuroglycopenia are surprisingly narrow. Subtle neuroelectrophysiological changes in cortical and brain stem function are evident at 2.9 mM. Insulin-dependent diabetes mellitus (IDDM) patients must rely heavily on their ability to secrete epinephrine to overcome a defective glucagon response. Unfortunately, this defense mechanism may diminish as disease duration increases, and may become further impaired by iatrogenic hypoglycemia accompanying insulin treatment. Commonly, the glucose level triggering adrenergic responses is shifted downward during intensive insulin therapy of IDDM. This may help explain why such patients release epinephrine and experience symptoms of hypoglycemia at a lower glucose level.

Adolescent↗
PubMed2004

Hypoglycemic brain damage.

Hypoglycemia was long considered to kill neurons by depriving them of glucose. We now know that hypoglycemia kills neurons actively from without, rather than by starvation from within. Hypoglycemia only causes neuronal death when the EEG becomes flat. This usually occurs after glucose levels have fallen below 1 mM (18 mg/dl) for some period, depending on body glycogen reserves. At the time that abrupt brain energy failure occurs, the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur and membrane breaks in the cell lead rapidly to neuronal necrosis. Significant neuronal necrosis occurs after 30 min of electrocerebral silence. Other neurochemical changes include energy depletion to roughly 25% of control, phospholipase and other enzyme activation, tissue alkalosis and a tendency for all cellular redox systems to shift towards oxidation. The neurochemistry of hypoglycemia thus differs markedly from ischemia. Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult.

Alkalosis↗
PubMed2003

Distal hypoglycemic neuropathy. An insulinoma-associated case, misdiagnosed as temporal lobe epilepsy.

Peripheral distal neuropathy associated with hypoglycemia secondary to insulinoma is quite rare. So far, less than 40 cases have been reported in literature. In this report, we describe a 50-year-old patient with insulinoma-polineuropathy and neuropsychiatric symptoms, interpreted as temporal lobe epilepsy, over the preceding 7 years. Due to the variability of the clinical presentation, diagnostic mistakes are frequent, and diagnosis of insulinoma is often delayed. Thus, the hypoglycemic nature of neuropathy can be lately recognized.

Blood Glucose↗
PubMed2000

Differential phosphorylation at Ser473 and Thr308 of Akt-1 in rat brain following hypoglycemic coma.

We analyzed both total Akt-1 and phosphorylation of Akt-1 at residues Ser473 and Thr308 (phospho-Akt-1(Ser474) and phospho-Akt-1(Thr308), respectively) in the outer and inner layers of cortex following 30 min of hypoglycemic coma by Western blot analyses and confocal microscopy. The total amount of Akt-1 was not altered in any area examined. Phospho-Akt-1(Ser474), however, increased significantly in both layers of cortex at 0 and 30 min of recovery, but returned to control level at 3 h of recovery. In the vulnerable area (outer layer of cortex), no upregulation of phospho-Akt-1(Thr308) was observed at any time points examined. In the resistant area like inner layer of cortex, however, phospho-Akt-1(Thr308) was significantly over the control level at 3 h of recovery. Confocal microscopy result indicates that most of phospho-Akt-1(Thr308) had already moved into nucleus at 3 h of recovery. Our results suggest that Akt-1, when phosphorylated at Thr308, may play a protective role for neurons in the resistant regions of the brain.

Amino Acid Sequence↗
PubMed1981

Variation in plasma ketone bodies during a 24-hour fast in normal and in hypoglycemic children: relationship to age.

The variations in blood ketone bodies, blood glucose, and insulin were studied in 19 normal and 14 hypoglycemic children, 4 months to 13 years of age, during a 24-hour fast. Except in four patients (two with hyperinsulinism and two with congenital defect in ketogenesis), a significant increase in blood ketone bodies was observed in both controls and patients. A progressive decrease in glucose concentrations was observed up to but not after 20 hours. A highly negative correlation between blood ketone bodies and blood glucose was found, with a large dispersion of blood ketone bodies, especially for those corresponding to the blood glucose between 45 and 65 mg/dl. This dispersion was consistently reduced in a homogenous age group of 4 to 6 years with similar glucose values. There was a positive correlation between age and blood glucose from hour 21 on, and an inverse relationship between age and blood ketone bodies from hour 15 on. The same high inverse relationship between age and blood ketone bodies was again observed when the variable of glucose concentration was factored out, demonstrating that the variation in blood ketone bodies is indeed related to age. These findings need to be taken into account in the interpretation of fasting blood ketone bodies, especially when used as an aid in the diagnosis of the various forms of childhood hypoglycemia, and of hypoketotic states.

Age Factors↗
PubMed1999

The effect of hypoglycemic seizures on cognitive function in children with diabetes: a 7-year prospective study.

Sixteen children with insulin-dependent diabetes mellitus were evaluated at diagnosis and after 1, 3, and 7 years. They showed significant declines in verbal but not visuospatial abilities, particularly if they had any seizures from hypoglycemia. At the 7-year assessment those with hypoglycemic seizures showed deficits on perceptual, motor, memory, and attention tasks.

Adolescent↗
PubMed1987

Diagnosis and treatment of hypoglycemic disorders.

Many other hypoglycemic states can be confused with an insulinoma. This article presents the diagnosis, localization, and therapy of these islet cell tumors. Also presented is a discussion of the role of nesidioblastosis in persistent hyperinsulinemic hypoglycemia in the neonate.

Adult↗
PubMed1982

Homologous and hybrid calcium complexes of A23187 and hypoglycemic sulfonylureas: nuclear magnetic resonance and conformational analysis.

Hypoglycemic sulfonylureas (e.g., gliclazide) are able to transport calcium across hydrophobic domains. Gliclazide and the ionophore A23187 act synergistically upon calcium transport. One calcium atom is complexed by either two molecules of sulfonylureas (or A23187) or one molecule each of sulfonylurea and A23187; the existence of such hybrid complexes has been documented by nuclear magnetic resonance. Conformation analysis of the calcium-gliclazide complex suggests close apposition of the toluyl groups in the gliclazide molecules.

Anti-Bacterial Agents↗
PubMed2000

Effects of the treatment with acarbose in elderly overweight type 2 diabetic patients in poor glycemic control with oral hypoglycemic agents or insulin.

The aim of this study was to evaluate the efficacy of acarbose, an inhibitor of alpha-glucosidase, on glycemic control in elderly overweight type 2 diabetic patients poorly controlled by oral hypoglycemic agents (OHA) or insulin. Our study included 22 overweight patients, 60-75-years-old, treated with OHA and/or insulin who, after a period of 4 weeks of controlled diet, showed a poor metabolic control. They were divided into two groups: Group I (nine patients) on OHA treatment; Group II (13 patients) undergoing treatment with insulin alone or in combination with OHA. Acarbose was administered to all the patients (100 mg three times a day at meal times) for 6 months in addition to their previous treatment. The addition of acarbose caused a significant reduction in both groups with regard to fasting glycemia (after 3 and 6 months, respectively, 20.7 and 21.9%, P<0.04 in Group I; 19.1 and 21.8%, P<0.04 in Group II), and postprandial glycemia (after 3 and 6 months, respectively, 41.6 and 42.5%, P<0.0001 in Group I; 35.6 and 38%, P<0.0006 in Group II). There was also a significant reduction in the values of HBA(1c) in Group I after 6 months of treatment (24.3%, P<0.05) and in Group II after 3 and 6 months (respectively 13.4%, P<0.02 and 20.6%, P<0.01). Three months after treatment with acarbose ended, fasting and postprandial glycemia and HBA(1c) values returned to original baseline values. In conclusion, the addition of acarbose to the OHA in elderly overweight type 2 diabetic patients poorly controlled by OHA or insulin regimes improved metabolic control.

Journal Article↗
PubMed1998

Hypoglycemic and hypotensive effects of 6-cyclohexyl-2'-O-methyl-adenosine, an adenosine A1 receptor agonist, in spontaneously hypertensive rat complicated with hyperglycemia.

Metabolic and cardiovascular effects of 6-cyclohexyl-2'-O-methyl-adenosine (SDZ WAG 994), a selective and orally-active adenosine A1 receptor agonist, were examined in spontaneously hypertensive rats (SHR) with hyperglycemia (SHR-DM). This model was made by the administration of streptozotocin (STZ; 60 mg/kg s.c.) to SHR 2 days after their birth. The serum glucose concentration and systolic/mean blood pressures (MBP) in 18-22-week-old rats were 14.7 +/- 0.8 mmol/1 and 153 +/- 3/124 +/- 3 mmHg in SHR-DM, 13.7 +/- 0.3 mmol/1 and 123 +/- 3/96 +/- 4 mmHg in normotensive with STZ (WKY-DM), 10.3 +/- 0.3 mmol/1 and 165 +/- 1/136 +/- 3 mmHg in non-treated (without STZ) SHR, and 10.0 +/- 0.3 mmol/1 and 115 +/- 3/90 +/- 4 mmHg in non-treated WKY, SDZ WAG 994 at 0.1 mg/kg p.o. lowered the serum glucose concentration, blood pressure and heart rate in SHR-DM. The effects were associated with the decrease in free fatty acid (FFA), triglyceride (TG), phospholipid (PL) and total cholesterol (TC) in serum of both SHR-DM and WKY-DM. On the contrary, the hypoglycemic effect was not found in WKY-DM, although the hypotensive effect was still observed. These data suggest that the risk factors for metabolic and cardiovascular complications in diabetes are reduced by SDZ WAG 994 through activation of adenosine A1 receptors in adipocyte.

Adenosine↗
PubMed1982

Ethanol-induced hypoglycemic coma in a child.

Reported is a case of ethanol-induced hypoglycemic coma in a 33-month-old boy after accidental ingestion of ethanol. Blood glucose was 10 mg% and blood ethanol was 71 mg%. He responded promptly to an IV bolus of 50% dextrose. The pathophysiology and clinical presentation of this not uncommon metabolic disorder are discussed. A plan for early recognition and management is presented.

Adult↗
PubMed1999

Hypoketotic hypoglycemic coma in a 21-month-old child.

We present the case of a 21-month-old child with hypoketotic hypoglycemic coma. The differential diagnosis initially included metabolic causes versus a toxicologic emergency (unripe ackee fruit poisoning). Using information obtained from the emergency department, the diagnosis was confirmed as the late-onset form of glutaric acidemia type II. This case illustrates the importance of emergency physicians in the diagnosis and management of children with inborn errors of metabolism.

Acidosis↗
PubMedDate not supplied

[Hypoglycemic hemiplegia. Apropos of a case].

An insulin-dependent 26-year-old woman was complaining of nocturnal attacks of transient right hemiplegia. Hypoglycemia was found to be present at the time of each attack, and further investigations showed that these neurological disorders were related to an overdose of insulin. The authors discuss the effects of hypoglycemia on the brain and the pathogenetic theory of "hypoglycemic hemiplegia", involving selective neuronal vulnerability, regional blood flow disturbances or underlying ischaemic disease.

Adult↗
PubMed1992

Cystic pancreatic glucagonoma in contact with insulinoma found in a hypoglycemic patient.

Cystic glucagonoma in contact with insulinoma was found in the pancreas of a 28-year-old female patient with characteristic hypoglycemic syndrome. Among six tumors in total detected in the tail of the resected pancreas, the largest solid tumor (2.5 cm in diameter) consisted mostly of insulin-containing cells with conspicuous amyloid deposition. Contiguous to this tumor, the second largest nodule, measuring 1.8 cm in diameter, showed cystic changes and consisted of glucagon-containing cells. High concentration of immunoreactive glucagon was demonstrated in the cystic fluid. In addition to the cystic changes of endocrine pancreatic tumors, simultaneous occurrence of glucagonoma in contact with insulinoma appears to be extremely rare and repeated episodes of hypoglycemia may contribute to its pathogenesis.

Adult↗
PubMed2000

Carbohydrate metabolism in temporal and persistent hypoglycemic chickens induced by insulin infusion.

In order to elucidate the regulatory mechanism of blood glucose concentrations specific to chickens, carbohydrate metabolism in the liver, muscle and kidney and metabolite concentrations in the blood were investigated in chickens with acute and persistent hypoglycemia. Acute and persistent hypoglycemia were experimentally induced by a single injection of insulin (8 U/kg BW) or by continuous infusion of insulin (22.5 U/kg BW/day) for 4 days. Non-esterified fatty acid (NEFA) concentration in plasma and D-3-hydroxybutyrate (3HB) concentrations in liver and muscle increased in the acute hypoglycemia. Plasma NEFA concentration and 3HB concentration in the blood and liver were not changed at day 3 of persistent hypoglycemia, while 3HB concentration in the muscle was decreased. Phosphofructokinase (PFK) activity in the liver tended to increase but PFK and pyruvate kinase (PK) activities were unchanged in acute hypoglycemia. In persistent hypoglycemia, increase of hepatic PFK activity at day 1 in which it was reversed at day 3, and a small increase of muscle PK activity were observed, while PK and phosphoenolpyruvate carboxykinase (PEPCK) activities in the liver and kidney were not significantly changed. These results show that in the persistent hypoglycemic chickens, hepatic glycolysis transiently increases, which is followed by a small decrease, while glycolysis in muscles and gluconeogenesis in the liver and kidney are not significantly changed.

3-Hydroxybutyric Acid↗
PubMed2001

Recurrent hypoglycemic hemiparesis and aphasia in an adolescent patient.

A 12-year-old diabetic female with right-side hemiparesis and aphasia occurring after a hypoglycemic episode is reported. Her clinical course improved over a 24-hour period, and further investigation revealed only electroencephalographic slowing, which was more prominent on the left. Ten months later, she had a recurrence of the same symptoms, which also resolved rapidly. This potential complication of hypoglycemia is often mistaken for a cerebrovascular accident.

Adolescent↗
PubMed1999

Diagnostic approach to adults with hypoglycemic disorders.

Optimal conditions for confirming the presence and accurately diagnosing the type of hypoglycemic disorder occur at the time of a spontaneous spell. Otherwise, dynamic testing to generate conducive conditions should be conducted in any patient with a history of neuroglycopenic symptoms, regardless of relation to meal ingestion. Specific criteria regarding beta-cell polypeptide concentrations are required to establish hyperinsulinemia. Sulfonylureas in plasma should be measured with sensitive assays. In complex cases, the selective arterial calcium test may be a useful dynamic test.

Antibodies↗