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At least 469 records · Page 26Linked to original sources
PubMed1994

Differential hypoglycemic effect of 2,5-anhydro-D-mannitol, a putative gluconeogenesis inhibitor, in genetically diabetic (db/db) and streptozotocin-induced diabetic mice.

2,5-Anhydro-D-mannitol (AM), a putative gluconeogenesis inhibitor, completely reversed the hyperglycemia in genetically diabetic (db/db) mice that exhibited hyperinsulinemia and enhanced hepatic gluconeogenic enzyme (glucose-6-phosphatase (G-6-Pase) and fructose-1,6-diphosphatase (F-1,6-DPase)) activities compared with the control +/+ mice. In contrast, AM only partially reversed the hyperglycemia of streptozotocin (STZ)-treated +/+ mice in which the hepatic gluconeogenic enzyme activities were enhanced to the same degree as in the db/db mice, whereas the blood insulin level was depressed. In the db/db mice, the STZ-treatment attenuated the hyperinsulinemia and exaggerated the hyperglycemia as well as the hepatic gluconeogenic enzyme activities, and it greatly reduced the hypoglycemic action of AM. Not only the dose-response curve of AM but also the time-course of the blood glucose level (expressed as % of pre-treatment value) following 320 mg/kg of AM were almost identical between +/+, STZ-treated +/+ and STZ-treated db/db mice. In the STZ-treated +/+ mice, a combination treatment of insulin (320 micrograms/kg) with AM (320 mg/kg) caused hypoglycemia that was greater than that induced by AM or insulin alone. On the other hand, in vitro studies with purified F-1,6-DPase revealed that phosphorylated AM (AM-1,6-diphosphate) but not AM itself inhibited the gluconeogenic enzyme activities. These results suggest that inhibition of gluconeogenesis is responsible, at least in part, for the hypoglycemic activity of AM. AM appears to inhibit hepatic gluconeogenic enzyme activities after being phosphorylated by an insulin-dependent mechanism.

Animals↗
PubMed1993

Insulin-like growth factors (IGF) I and II and IGF binding proteins 1, 2 and 3 during low-dose growth hormone (GH) infusion and sequential euglycemic and hypoglycemic glucose clamps: studies in GH-deficient patients.

To evaluate the short-term effects of growth hormone (GH), insulin and different levels of glycemia on insulin-like growth factors (IGF) I and II and IGF binding proteins (IGFBP) 1, 2 and 3, we studied six GH-deficient adolescents during a night and the following day in the postabsorptive (basal) state followed by sequential euglycemic (5 mmol/l) and hypoglycemic (3 mmol/l) glucose clamps concomitant with an intravenous infusion (starting at 24.00 h) of GH (35 micrograms/h) or saline. Current GH therapy was withdrawn 24 h prior to each study. Nocturnal levels of IGF-I, IGF-II, IGFBP-2 and IGFBP-3 remained stable during both studies. Nocturnal serum IGFBP-1 increased and correlated inversely with insulin in both studies. Regression analysis revealed a significant inverse correlation between mean nocturnal IGFBP-2 and IGFBP-3 levels. During the daytime, serum IGF-I declined slowly during saline infusion, whereas serum IGF-II remained stable in both studies. Serum IGFBP-1 displayed a gradual significant decline during the basal state and the euglycemic and hypoglycemic clamps seemed to be unaffected by GH levels. By contrast, serum IGFBP-2 remained stable during the same period in both the GH and the saline study. Serum IGFBP-3 declined insignificantly during the daytime in the saline study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Hypoglycemic coma masquerading thyrotoxic storm.

A 59-year-old woman was hospitalized in hypoglycemic coma. Although hypoglycemia was promptly reversed, she was in a somnolent, restless state with tachycardia, tremor, profuse sweating, and high body temperature. Thyrotoxic storm was highly suspected and vigorous antithyroid regimens gradually brought her up to normal mental and cardiovascular states in several days. However, profound generalized myopathy necessitated the maintenance with a respirator. One month later, an episode of angina pectoris was followed by generalized convulsion, coma, and death in a few days. Neuroimaging study disclosed posterior leukoencephalopathy syndrome. This case is instructive in that hypoglycemic coma may masquerade the major symptomatology of thyrotoxic storm, and that profound myopathy and angiopathic or angiospastic processes of the brain and the heart may interfere with the outcome.

Brain↗
PubMed1975

Prevention of hypoglycemic attacks by propranolol in a patient suffering from insulinoma.

An insulinoma was diagnosed in a fifty-seven-year-old woman suffering from frequent hypoglycemic attacks. Propranolol--a beta-adrenergic blocker--in a dose of 80 mg. per day effectively prevented recurrent hypoglycemic attacks. It also corrected the basal hyperinsulinemia as well as the increased insulin secretion which results from stimulation with glucose or arginine.

Adenoma, Islet Cell↗
PubMed1982

Prolonged hypoglycemic effect in diabetic dogs due to subcutaneous administration of insulin in liposomes.

The biologic action of insulin entrapped in liposomes (phospholipid vesicles) has been investigated following subcutaneous injection to dogs made diabetic with a combination of alloxan and streptozotocin. The fats of the liposomally entrapped material was determined by injecting rats subcutaneously with either 125I-insulin or the labeled polysaccharide 14C-inulin, incorporated in liposomes labeled with 3H-cholesterol. Injection of liposome insulin (0.75 U/kg) to five diabetic dogs resulted in a mean (+/- SEM) blood glucose fall from 16.4 +/- 0.8 to 2.9 +/- 0.4 mmol/L. The glucose level had still not returned to baseline after 24 h and, correspondingly, immunoreactive insulin (IRI) could still be detected in frozen and thawed plasma 24 h after injection. In contrast, the hypoglycemic effect of the same dose of free insulin with or without empty liposomes virtually ended within 8 h and IRI levels returned to baseline by 3 h after injection. In experiments on rats with liposomally entrapped 125I-insulin or 14C-inulin the proportion of the injected dose of tracer recoverable by excision of the injection site remained constant after about 1 h and 70% of the dose was still fixed in subcutaneous tissue for at least 5 h thereafter. When the plasma collected 3 h after subcutaneous injection of labeled liposomes containing 125I-insulin was passed through a column of Sepharose 6B, 50-75% of the 125I-activity was found in the fractions associated with intact liposomes. One possibility for the persistence of the hypoglycemic effect and of measurable IRI following injection of liposome insulin could be the presence of intact liposomes in the circulation for many hours after adsorption had ceased.

Animals↗
PubMed1983

Pulsatile insulin has greater hypoglycemic effect than continuous delivery.

The relative hypoglycemic effects of pulsatile versus steadily infused insulin have been examined in six normal subjects in whom pancreatic insulin output was suppressed by somatostatin-14. Soluble insulin was infused continuously overnight on one occasion and on another occasion the same quantity was given in pulses of 2-min duration with a gap of 11 min. The mean plasma glucose concentrations were lower when pulsed insulin was given [mean for the last hour: 4.66 +/- 0.08 mmol/L (+/- SEM) versus 5.53 +/- 0.06 mmol/L (+/- SEM) for steady infusion], diverging significantly (P less than 0.05 paired t test) 7 h after the start of the study. The specific binding of 125I(A14)mono-iodo-insulin to monocytes was greater after pulsed insulin (2.9% with pulsed versus 2.4% with steadily infused insulin at tracer-only point; P less than 0.02 paired t test). Thus, intravenous insulin has greater hypoglycemic effect when pulsed, possibly mediated by greater insulin receptor binding.

Adult↗
PubMed1988

Hypolipidemic, antiobesity, and hypoglycemic-hypoinsulinemic effects of beta,beta'-methyl-substituted hexadecanedioic acid in sand rats.

Treatment of male sand rats kept on a balanced laboratory chow diet ad libitum with beta,beta'-tetramethyl-substituted hexadecanedioic acid (MEDICA 16) resulted in a hypolipidemic effect accompanied by an extensive reduction in adiposity, with a concomitant hypoglycemic-hypoinsulinemic effect. The overall effect was sustained as long as the drug was administered. The hypolipidemic effect of MEDICA 16 consisted of a 70 and 40% decrease in plasma triacylglycerols and cholesterol, respectively, and resulted from inhibition of liver lipogenesis and cholesterogenesis. Adipose reduction by MEDICA 16 treatment or calorie restriction consisted of a 75-90% decrease in the perirenal, omental, epididymal, and subcutaneous fat, with a 50% decrease in liver neutral lipids. The reduction in adiposity was accounted for by a respective decrease in the lipid content of individual adipocytes, with a concomitant decrease in the number of adipocytes of selected adipose tissues. The decrease induced in adiposity by MEDICA 16 treatment could not be accounted for by anorectic or cathartic effects of the drug. The hypoglycemic-hypoinsulinemic effect of MEDICA 16 consisted of amelioration of the tolerance of glucose with normalization of plasma insulin. It was accompanied by an eightfold increase in the number of insulin receptors in epididymal adipocytes, which was, however, counteracted by a decrease in their affinity for insulin. The receptor and postreceptor effects exerted by MEDICA 16 were similar to those of calorie restriction. The overall effect of MEDICA 16 in sand rats may reflect the pharmacological potential of MEDICA compounds in pathological hyperlipidemic-obesity-diabetic syndromes.

Adipose Tissue↗
PubMed1991

Multifactorial origin of hypoglycemic symptom unawareness in IDDM. Association with defective glucose counterregulation and better glycemic control.

To assess potential relationships between unawareness of hypoglycemic symptoms and both defective glucose counterregulation and therapy-associated altered glycemic thresholds, symptoms and hormonal responses to hypoglycemia were quantitated during standardized insulin infusion tests in 41 patients with insulin-dependent diabetes mellitus (IDDM). The glycemic thresholds for both neurogenic and neuroglycopenic symptoms (and those for both epinephrine and pancreatic polypeptide release) were at lower plasma glucose concentrations in both patients with defective (n = 9, 22%) and those with adequate glucose counterregulation and, among the latter, in patients with lower compared with higher glycosylated hemoglobin levels. The data are consistent with the concept that both defective glucose counterregulation and improved glycemic control contribute to excessive hypoglycemia in IDDM by reducing awareness of symptoms of developing hypoglycemia and by impairing physiological defenses against hypoglycemia. Thus, hypoglycemic symptom unawareness is multifactorial in origin and may be partly reversible.

Awareness↗
PubMed2003

Local lactate perfusion of the ventromedial hypothalamus suppresses hypoglycemic counterregulation.

We have previously reported that a glucosensor integrating hormonal responses to hypoglycemia is located in the ventromedial hypothalamus (VMH) and that local VMH glucose perfusion blocks counterregulatory hormone responses. To determine whether the by-product of glucose metabolism, lactate, can function within the VMH as an alternative for glucose, we delivered lactate locally to the VMH, during systemic hypoglycemia. For this purpose, we combined bilateral VMH microdialysis perfusion (metabolically active L-lactate or its nonmetabolizable D-isomer) with a euglycemic-hypoglycemic clamp in conscious chronically catheterized Sprague-Dawley rats. Local VMH perfusion with L-lactate decreased counterregulatory hormone responses to hypoglycemia by 80-85% as compared with the nonmetabolizable D-lactate control. Moreover, hormonal suppression with L-lactate was accompanied by an approximate fourfold increase in the amount of exogenous glucose infused to maintain a stable hypoglycemic plateau (P < 0.05). In conclusion, the glucose-sensing mechanism in the VMH responds to lactate and, thus, is not specific for glucose. This implies that the VMH may act as a fuel sensor rather than as a glucose sensor.

Animals↗
PubMed1994

Hypoglycemic activity of glyburide (glibenclamide) metabolites in humans.

OBJECTIVE: To assess the hypoglycemic effect and the insulin-releasing effect of the main glyburide (glibenclamide) metabolites 4-trans-hydroxy-glibenclamide (M1) and 3-cis-hydroxy-glibenclamide (M2) in humans. RESEARCH DESIGN AND METHODS: Eight healthy subjects participated in a placebo-controlled, randomized, single-blind crossover study with five single-dose tests, 3 months apart: 3.5 mg glibenclamide (Gb) orally, 3.5 mg Gb intravenously, 3.5 mg M1 intravenously, 3.5 mg M2 intravenously, and placebo intravenously, each in the fasting state. Standardized meals were given 0.5 and 5.5 h after each medication. Blood glucose levels were measured by a glucose oxidase method, and serum insulin concentrations were analyzed by a specific immunoassay. RESULTS: Blood glucose levels during the first 5 h were significantly lowered not only by Gb but also by M1 and M2. The mean +/- SE blood glucose reductions (versus placebo) expressed as percent of area under the curve (AUC) (0-5 h) were 18.2 +/- 3.3% for M1, 12.5 +/- 2.3% for M2, 19.9 +/- 2.1% for intravenous Gb, and 23.8 +/- 1.2% for Gb orally. Serum insulin levels were significantly increased by Gb as well as by M1 and M2. and M2. CONCLUSIONS: The two main metabolites of glyburide (glibenclamide) have a hypoglycemic effect in humans, which is due to increased insulin secretion.

Administration, Oral↗
PubMedDate not supplied

Incidence of hypoglycemic episodes in diabetic patients under continuous subcutaneous insulin infusion and intensified conventional insulin treatment: assessment by means of semiambulatory 24-hour continuous blood glucose monitoring.

The incidence and magnitude of hypoglycemia (i.e., blood glucose values less than 50 mg/dl) were assessed by continuous blood glucose monitoring over 24 h in 10 insulin-dependent diabetic (IDD) patients treated with continuous subcutaneous insulin infusion (CSII) and 9 IDD patients under intensified conventional treatment (ICT). A newly developed, battery-powered blood glucose monitor was employed. Patients were thus enabled to move freely in the hospital premises. Despite similar quality of previous blood glucose control (HbA1: 8.0 +/- 0.05% CSII versus 8.0 +/- 0.3% ICT, mean +/- SEM), the obtained profiles showed better regulation under CSII treatment (mean blood glucose [MBG], 99.6 +/- 10.0 versus 133.1 +/- 7.4 mg/dl; M-value, 12.3 +/- 3.5 versus 26.2 +/- 4.1; mean amplitude of glycemic excursion [MAGE], 71.9 +/- 8.7 versus 132.9 +/- 14.2 mg/dl; CSII versus ICT, mean +/- SEM). The incidence of blood glucose values less than 50 mg/dl was 9/10 patients (CSII) and 5/9 patients (ICT). In both groups, hypoglycemia was most frequent at noon and was related to elevated pre- and postprandial free insulin levels. Patients became aware of hypoglycemia only in 6/23 episodes (CSII) and 6/8 episodes (ICT). Our data indicate that CSII as well as ICT may result in postprandial hyperinsulinemia leading to frequent hypoglycemic episodes of variable length, reassessing the traditional experience of close correlation between aggressive insulin therapy and enhanced hypoglycemic risk.

Adolescent↗
PubMedDate not supplied

Glucagon constant-rate infusion: a novel strategy for the management of hyperinsulinemic-hypoglycemic crisis in the dog.

A six-year-old, spayed female, cocker spaniel was presented for hypoglycemic seizures. Hypoglycemia with concomitant hyperinsulinemia suggested an insulin-secreting tumor. Pancreatic masses were resected, and insulinoma was diagnosed. Six weeks later, the dog presented in hyperinsulinemic-hypoglycemic crisis (HHC). The dog was initially stabilized with intravenous dextrose boluses and infusions, but seizure activity recurred and persisted. A glucagon constant-rate infusion (GCRI) was initiated, and neurological signs quickly resolved. Dextrose was withdrawn over 24 hours, and euglycemia was maintained by GCRI alone. Despite aggressive medical management including the use of prednisone, diazoxide, bovine somatotropin, and streptozocin, the dog presented on two subsequent occasions in HHC and both times was rapidly stabilized with GCRI alone. In this dog, GCRI was a fast, safe, and effective method of achieving and maintaining euglycemia despite intractable hyperinsulinism. The clinical use of GCRI merits further investigation for management of HHC in veterinary species.

Animals↗
PubMed1998

Search for Extrapancreatic Effects of New Oral Hypoglycemic Agent A-4166: 1. Oral Glucose Tolerance Tests in Normal and Hereditary Insulin Resistant Rats.

OBJECTIVE: To test the effect of new oral hypoglycemic compound A-4166 on insulin secretion during oral glucose challenge in normal and hereditary non-obese, hypertriglyceridemic, insulin resistant and hypertensive rats fed either a normal or high fat diet. METHODS: The rats used were 15 weeks old males of Wistar Charles River strain (controls) and Wistar-derived hereditary hypertriglyceridemic (hHTg) rats of our own colony. They were fed either basal (12 cal% of fat) or high fat diet (70 cal% fat). After 3 weeks of feeding the above diets, the oral glucose tolerance tests (2 g/kg) were carried out in unrestrained conscious rats kept in special metabolic cages after overnight fasting and ten minutes after the administration of A-4166 (100 mg/kg) or placebo by the stomach tube. Plasma glucose, triglycerides, free fatty acids and insulin levels were measured by routine analytical methods. RESULTS: High fat diet feeding resulted in an increase in fasting plasma insulin in both rat strains, while fasting plasma glucose in high fat diet fed animals remained unchanged as compared to those fed basal diet. No differences in the fasting FFA levels were found. The glucose area under curve (AUC) did not differ between the two strains used and high fat diet resulted in a higher glucose AUC in both strains. The administration of A-4166 improved the glucose tolerance in all animals, namely in those fed the basal diet. Insulin AUC showed very similar pattern in both rat strains proving the stimulatory effect of A-4166 on insulin secretion during an oral glucose challenge. High fat feeding resulted in an impairment of insulin action, but the administration of A-4166 restored the antilipolysis in both strains to the normal range. CONCLUSIONS: The previously reported hypoglycemic action of A-4166 resulting from the increased insulin secretion was confirmed. Moreover, some beneficial action of A-4166 on antilipolysis in vivo was demonstrated.

Journal Article↗
PubMed1975

Mechanism of "hypoglycemic" cataract formation in the rat lens. I. The role of hexokinase instability.

Lenses from 100 gram albino rats remain clear and possess normal levels of Na+, K+, ATP, and hexokinase activity for 20 hours incubated in medium containing 12 mM glucose. Below 2.0 mM glucose, a cataract forms and there is an abrupt rise in lens Na+ and wet weight, a fall in lens K+, ATP, and hexokinase activity. The cataract is a thin lamellar opacity involving the anterior and posterior surfaces of the lens. If the lens is deprived of glucose for 48 hours, a nuclear cataract forms; the cortex between the superficial lamellar opacity and the nucleus being clear. This experimental cataract bears a striking resemblance to the hypoglycemic cataract seen in children. The thermal deactivation of hexokinase follows rapidly upon the depletion of its substrates (ATP and glucose) and is a primary factor leading to cataract formation. This was established by incubating the lens with 2-deoxyglucose, a competitive inhibitor of lens hexokinase. This compound blocks the entry of glucose into the glycolytic sequence. The cataract formed in its presence is identical morphologically and biochemically to that observed in a glucose-free medium. The effects of 2-deoxyglucose are prevented by increasing the glucose level; this rules out a direct toxic influence of 2-deoxyglucose and further supports the primary role of hexokinase thermolability in the etiology of this experimental cataract. This in vitro system appears to be an excellent experimental model for the study of the human hypoglycemic cataract.

Adenosine Triphosphate↗
PubMed2002

Event related P300 potential in NIDDM patients without cognitive impairment and its relationship with previous hypoglycemic episodes.

OBJECTIVES: The purpose of this study was to evaluate the ERP P300 in non insulin dependent diabetes mellitus (NIDDM) patients without cognitive impairment and the relationship with clinical variables, the presence of retinopathy and previous hypoglycemic episodes. METHODS: NIDDM patients (N=44) without evidence of cognitive impairment and controls (N=17) were studied clinically and with ancillary exams and the ERPs P300 were recorded. Patients were examined clinically and with the Folstein Mini-Mental Examination (MMSE) for cognitive function and all patients showed a score higher than 26 (maximal value=30). Previous hypoglycemia was evaluated through a questionnaire establishing the number of episodes and the symptoms of hypoglycemia in a scale scoring from zero to 15. RESULTS: ERP P300 latencies were significantly higher in NIDDM patients than in controls (p<0.03). ERP P300 measures were significantly related to age (Pearson, p<0.01) and not to metabolic variables, disease duration or the presence of retinopathy. Severity of hypoglycemia was not associated to ERP P300 latency. CONCLUSIONS: Our study supports the evidence that NIDDM patients, without signs of nervous system involvement, have ERP P300 alterations and this is not related to retinopathy, metabolic variables or previous hypoglycemic episodes. Chronic hyperglycemia may alter brain glucose transport and increase tolerance to hypoglycemia effects in the nervous system.

Adult↗
PubMed2002

Hypoglycemic effect of aqueous extract of Ammi visnaga in normal and streptozotocin-induced diabetic rats.

The effect of the aqueous extract of Ammi visnaga (Apiaceae) on blood glucose levels was investigated in fasting normal and streptozotocin-induced diabetic rats after single and repeated oral administration. The aqueous extract of Ammi visnaga (AV) at a dose of 20 mg/kg significantly reduced blood glucose in normal rats six hours after a single oral administration (P < 0.005) and nine days after repeated oral administration (P < 0.05). This hypoglycemic effect is more pronounced in streptozotocin (STZ) diabetic rats (P < 0.001). Acute toxicity (LD50) and general behavioural effects of an aqueous extract of AV fruits was studied in mice. The LD50 of intraperitoneal (i.p.) and oral administration was 3.6 and 10.1 g/kg, respectively. These findings suggest that the aqueous extract of AV possess significant hypoglycemic effect in both normal and STZ diabetic rats and support, therefore, its claimed clinical use by the Moroccan population.

Journal Article↗
PubMed1990

[Transient hypoglycemic hemiplegia due to insulin autoimmune syndrome--a case report].

Hypoglycemia causes a variety of neurologic symptoms, and yet it is rarely responsible for such a sudden, focal neurologic deficit as hemiplegia. Herein we described a rare case of what was believed to be transient hypoglycemic hemiplegia. An 80-year-old woman was admitted to the hospital on June 10, 1988, following frequent episodes of abnormal behavior and transient weakness of the right extremities. These symptoms, similar to those of cerebrovascular diseases, characteristically occurred early in the morning and disappeared after breakfast. On admission no definite abnormalities were disclosed on neurologic examination. Neuroradiological evaluations by CT, cerebral angiography and single photon emission CT failed to demonstrate abnormalities. The patient remained stable until the following morning, when she suddenly became restless and confused and developed total aphasia and the right hemiplegia. The blood sugar was estimated to be 34 mg/dl and electroencephalogram (EEG) showed continuous slow wave activities involving the bilateral fronto-parietal region. Intravenous injection of glucose solution instantaneously resulted in disappearance of both neurologic symptoms and EEG abnormality. Serum insulin level was found extremely increased ranging from 7000 to 8000 microU, eventually leading to a diagnosis of insulin autoimmune syndrome. Hemiplegia due to hypoglycemic attack was reviewed in the literature, and the pathogenesis and EEG findings were also discussed.

Aged↗
PubMedDate not supplied

[Hypoglycemic action of Opuntia streptacantha Lemaire: study using raw extracts].

To find out the extent of the hypoglycemic effect of crude extracts of Opuntia streptacantha eight patients with type II diabetes mellitus were studied. Five tests were performed to each patients with the intake of (A) supernatant, (B) precipitate, (C) complete homogenate of 500 g of crude O. streptacantha stem (D) 400 ml of water, and (E) 500 g of broiled Opuntia stems. Serum glucose levels were measured at 0,30,60,120 and 180 minutes. Crude extracts did not cause a significant decrease of glycemia, and the results were similar to the water control test (P greater than 0.05). The intake of broiled Opuntia stems caused a significant decrease of serum glucose level, that reached 48.3 +/- 16.2 mg/dl lower than basal values at 180 minutes (P less than 0.01). Perhaps heating of O. streptacantha is necessary to obtain the hypoglycemic effect.

Administration, Oral↗