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PubMed1983

Lactate reverses insulin-induced hypoglycemic stupor in suckling-weanling mice: biochemical correlates in blood, liver, and brain.

The recovery of weanling mice from insulin-induced hypoglycemic stupor-coma after injection of sodium -L(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the beta-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in alpha-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO-3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and alpha-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Alterations in tissue glucose uptake during the hyperglycemic and hypoglycemic phases of sepsis.

The purpose of the present study was to characterize the alterations in tissue glucose uptake during the hyperglycemic, euglycemic, and hypoglycemic phases of peritonitis. Rats had vascular catheters implanted, and sepsis was induced by cecal ligation and puncture. Rates of whole-body glucose appearance (Ra), disappearance (Rd), and metabolic clearance (MCR) were determined by the constant infusion of 3H-glucose, and in vivo glucose uptake (Rg) by individual tissues was assessed by using 14C-deoxyglucose. During the hyperglycemic phase of sepsis (2 h), glucose Ra and Rd were increased, but glucose MCR was unaltered. In contrast, during the euglycemic phase (6 h), the sepsis-induced increase in glucose Ra and Rd was associated with an elevation in the MCR. Finally, during the hypoglycemic phase (24 h), sepsis decreased glucose Ra and Rd and the glucose MCR. The sepsis-induced changes in Rg for skeletal muscle and adipose tissue mimic those seen for the whole body at each time point. Rg for skin and intestine was elevated at 2 h and 6 h but was not different from control values at 24 h. In contrast, the Rg for liver, lung, and spleen was increased at all 3 time points. In a second study, there was no difference in Rg for any tissue between 2-h septic rats and control animals in which blood glucose and insulin levels were artificially elevated to the same degree. In a third study, the prevailing glucose and insulin levels in control animals were decreased, by injection of the gluconeogenic inhibitor 3-mercaptopicolinic acid, to levels seen in 24-h septic rats. There was no difference in the Rg for muscle and adipose tissue between 24-h septic rats and hypoglycemic insulinopenic control animals. However, the Rg for liver, lung, and spleen remained elevated in 24-h septic rats, compared with hypoglycemic insulinopenic control values. These data indicate that the increased tissue glucose uptake observed during the early phase of sepsis is a consequence of concomitant changes in plasma glucose and insulin. In contrast, during the euglycemic and hypoglycemic stages of sepsis, glucose uptake in macrophage-rich tissues remains elevated and is independent of changes in glucose and insulin.

Animals↗
PubMed1984

Hypoglycemic episodes during continuous subcutaneous insulin infusion: decreased frequency but increased susceptibility.

There has been concern regarding the susceptibility of patients on continuous subcutaneous insulin infusion (CSII) to hypoglycemic episodes. This study has examined glycemic control, the frequency of hypoglycemic reactions and the counterregulatory response to an IV insulin infusion fo 2.4 units per hour in five brittle insulin-dependent diabetics before and during CSII. CSII was associated a significant reduction in glycosylated hemoglobin, standard deviation of blood glucose estimations and daily insulin dosage. The frequency of symptomatic hypoglycemic reactions was reduced (mean 14/4 weeks pre CSII, 5/4 weeks post CSII, p less than 0.05). However, after CSII the IV insulin caused a more rapid fall in blood glucose from the physiological to the hypoglycemic range while growth hormone and cortisol responses were both reduced (p less than 0.05) and the deficient glucagon response was not improved. Thus, although the frequency of reported hypoglycemic reactions was reduced by CSII, susceptibility to hypoglycemia due to excess insulin delivery was enhanced, owing to increased insulin sensitivity and/or additional impairment of the counterregulatory response.

Adult↗
PubMed1987

Ketogenesis in hypoglycemic neonates. Carnitine and dicarboxylic acids in neonatal hypoglycemia.

Since hypoglycemic neonates do not exhibit compensative ketosis, we investigated the possible involvement of carnitine deficiency or omega-oxidation in neonatal hypoglycemia. In a first group of 49 neonates, serum free fatty acid, acetoacetate and beta-hydroxybutyrate concentrations were similar in hypoglycemic and normoglycemic neonates. Serum free carnitine concentrations did not show any difference in the hypoglycemic small-for-date infants (median 40 mumol/l, range 16-92 mumol/l) compared to the normoglycemic small-for-date infants (median 30 mumol/l, range 8-64 mumol/l). In a second group of 45 neonates, urinary excretion of dicarboxylic acids (adipic, suberic, sebaric and succinic acids) was similar in hypoglycemic infants compared to normoglycemic neonates. Despite the limitations of interpretation of free carnitine determination, these data do not suggest an impaired beta-oxidation by carnitine depletion or an enzymatic defect in hypoglycemic neonates.

3-Hydroxybutyric Acid↗
PubMed2005

Hypoglycemic and hypotensive effects of Psidium guajava Linn. (Myrtaceae) leaf aqueous extract.

The leaf of Psidium guajava Linn. (family, Myrtaceae) is used traditionally in African folk medicine to manage, control, and/or treat a plethora of human ailments, including diabetes mellitus and hypertension. In order to scientifically appraise some of the anecdotal, folkloric, ethnomedical uses of P. guajava Linn., the present study was undertaken to investigate the hypoglycemic and hypotensive effects of P. guajava leaf aqueous extract (PGE, 50-800 mg/kg) in rat experimental paradigms. The hypoglycemic effect of the plant's extract was examined in normal and diabetic rats, using streptozotocin (STZ)-induced diabetes mellitus model. Hypertensive Dahl salt-sensitive rats were used to investigate the hypotensive (antihypertensive) effect of the plant's extract. Chlorpropamide (CPP; 250 mg/kg, p.o.) was used as the reference hypoglycemic agent for comparison. Acute oral administrations of the plant's extract (PGE; 50-800 mg/kg, p.o.) caused dose-related, significant (p < 0.05-0.001) hypoglycemia in normal (normoglycemic) and STZ-treated, diabetic rats. Moreover, acute intravenous administrations of the plant's extract (PGE, 50-800 mg/kg i.v.) produced dose-dependent, significant reductions (p < 0.05-0.001) in systemic arterial blood pressures and heart rates of hypertensive, Dahl salt-sensitive rats. Although the exact mechanisms of action of the plant's extract still remain speculative at present, it is unlikely that the extract causes hypotension in the mammalian experimental animal model used via cholinergic mechanisms, since its cardiodepressant effects are resistant to atropine pretreatment. The numerous tannins, polyphenolic compounds, flavonoids, pentacyclic triterpenoids, guiajaverin, quercetin, and other chemical compounds present in the plant are speculated to account for the observed hypoglycemic and hypotensive effects of the plant's leaf extract. However, the results of this experimental animal study indicate that the leaf aqueous extract of P. guajava possesses hypoglycemic and hypotensive properties, and thus lend pharmacological credence to the suggested folkloric, ethnomedical uses of the plant in the management or control of adult-onset, type 2 diabetes mellitus and hypertension in some rural African communities.

Animals↗
PubMed1997

A case of a non-insulin dependent diabetic patient with regular spontaneous hypoglycemic attacks, which were due to insulin-binding antibodies induced by human insulin therapy.

A 74-year-old diabetic patient had been treated with oral hypoglycemic agents from the age of 40 years until the age of 72, when his treatment regimen was changed to human insulin. He began experiencing hypoglycemic attacks 14 months after the initiation of insulin therapy. He continued to experience hyperglycemia every morning and hypoglycemia every day at 5:30 p.m. even after insulin therapy was withdrawn. His plasma levels of C-peptide immunoreactivity, total and free immunoreactive insulins were 4.2 ng/ ml, 740 microU/ml and 141.8 microU/ml, respectively. His 125I-insulin binding rate was 94.4%. These findings suggest that his hypoglycemic attacks may have been due to insulin antibodies. Analysis revealed that insulin binding antibodies belonged to IgG with kappa light chains. The patient's genotype was HLA-DR4. He had not received animal insulin or any medications containing a sulfhydryl group. Although the IgG antibody was produced against injected human insulin, his HLA type and the characteristics of his antibodies resembled those of a patient with insulin autoimmune syndrome (IAS). We hypothesize that this patient represented a rare instance of a patient constitutionally similar to a patient with IAS, but whose hypoglycemic attacks resulted from the antibodies induced by the administration of human insulin. This case seems to be the first one with hypoglycemic attacks due to anti-human insulin antibody produced by human insulin therapy.

Aged↗
PubMed1995

Effect of hypoglycemic stress on the pars intermedia of the mouse pituitary gland: an ultrastructural analysis.

The present study was made to clarify the relationship between functions of the pars intermedia of the mouse pituitary gland and hypoglycemic stress. Morphometrical analysis of the ultrastructures of the pars intermedia cells showed (1) a rise in the percentage volume of rough endoplasmic reticulum (r-ER) indicative of an increase in protein synthesis, (2) an increase in the number of Golgi granules per unit Golgi area showing an induction of granule-forming activity and (3) a decrease in the numerical density of secretory granules reflecting a release of the secretory granules. These findings suggest that hypoglycemic stress induced by daily treatment with insulin or restriction of food intake was able to elicit heightened secretory activity of the pars intermedia cells of the mouse pituitary gland. However, acute hypoglycemic stress induced by food deprivation did not cytologically affect the pars intermedia. These observations suggest that repeated hypoglycemic stress, rather than acute hypoglycemic stress, may be a natural physiological stimulus of the pars intermedia of the mouse pituitary gland.

Animals↗
PubMed1996

Impact of recent antecedent hypoglycemia on hypoglycemic cognitive dysfunction in nondiabetic humans.

To test the hypothesis that glycemic thresholds for hypoglycemic cognitive dysfunction, like those for neuroendocrine responses to and symptoms of hypoglycemia, shift to lower plasma glucose concentrations after recent antecedent hypoglycemia, 16 healthy young adult subjects (7 women and 9 men) were studied on two separate occasions in random sequence, once with hyperinsulinemic hypoglycemia (2.6 +/- 0.1 mmol/l, 47 +/- 1 mg/dl) and once with otherwise identical hyperinsulinemic euglycemia (4.8 +/- 0.1 mmol/l, 86 +/- 5 mg/dl) between 1430 and 1630. Neuroendocrine, symptomatic, and cognitive responses to hyperinsulinemic stepped hypoglycemic (4.7, 4.2, 3.6, 3.0, 2.8, 2.5, and 2.2 mmol/l; 85, 75, 65, 55, 50, 45, and 40 mg/dl) clamps were quantitated the following morning on both occasions. Cognitive function tests included measures of information processing (Serial Addition), attention (Stroop Arrow Word), pattern recognition and memory (Delayed Non-Match to Sample), and declarative memory (Paragraph Recall). As expected, plasma glucagon (P = 0.0094), epinephrine (P = 0.0063), and pancreatic polypeptide (P = 0.0046) responses to stepped hypoglycemia were reduced significantly, and symptomatic responses tended to be reduced after afternoon hypoglycemia. Performance on the cognitive function tests deteriorated (P < 0.0001) during stepped hypoglycemic clamps, but there were no significant overall effects of antecedent hypoglycemia on hypoglycemic cognitive dysfunction. Although deterioration was reduced (P < 0.05) from the 2.8 mmol/l (50 mg/dl) to the 2.5 mmol/l (45 mg/dl) steps on the Serial Addition and Delayed Non-Match to Sample tasks after afternoon hypoglycemia, comparable differences were not found on the Stroop Arrow Word or Paragraph Recall tasks. Thus, glycemic thresholds for hypoglycemic cognitive dysfunction, unlike those for neuroendocrine responses to and symptoms of hypoglycemia, do not seem to shift to substantially lower plasma glucose concentrations after recent antecedent hypoglycemia in nondiabetic humans.

Adolescent↗
PubMed2002

Intrahepatic islet transplantation in type 1 diabetic patients does not restore hypoglycemic hormonal counterregulation or symptom recognition after insulin independence.

Islet allotransplantation can provide prolonged insulin independence in selected individuals with type 1 diabetes. Whether islet transplantation also restores hypoglycemic counterregulation is unclear. To determine if hypoglycemic counterregulation is restored by islet transplantation, we studied hormone responses and hypoglycemic symptom recognition in seven insulin-independent islet transplant recipients using a 3-h stepped hypoglycemic clamp, and compared their responses to those of nontransplanted type 1 diabetic subjects and nondiabetic control subjects. Glucagon responses of islet transplant recipients to hypoglycemia were significantly less than that observed in control subjects (incremental glucagon [mean +/- SE]: -12 +/- 12 vs. 64 +/- 22 pg/ml, respectively; P < 0.05), and not significantly different from that of nontransplanted type 1 diabetic subjects (-17 +/- 10 pg/ml). Epinephrine responses and symptom recognition were also not restored by islet transplantation (incremental epinephrine [mean +/- SE]: 195 +/- 128 [islet transplant recipients] vs. 238 +/- 73 [type 1 diabetic subjects] vs. 633 +/- 139 pg/ml [nondiabetic control subjects], P < 0.05 vs. control; peak symptom scores: 3.3 +/- 0.9 [islet transplant recipients] vs. 3.1 +/- 1.1 [type 1 diabetic subjects] vs. 6.7 +/- 0.8 [nondiabetic control subjects]). Thus the results indicate that despite providing prolonged insulin independence and near-normal glycemic control in these patients with long-standing type 1 diabetes, hypoglycemic hormonal counterregulation and symptom recognition were not restored by intrahepatic islet transplantation.

Adult↗
PubMed1988

Insulin controlled-release microcapsules to prolong the hypoglycemic effect in diabetic rats.

A solvent evaporation process was employed for preparing insulin microcapsules by using biodegradable polymers [polylactic acid (PLA), HP-55] and non-biodegradable polymers [ethylcellulose (EC), ethylenevinyl acetate (EVA)]. The release behavior of insulin microcapsules in pH 7.4 phosphate buffer solution was undertaken by a continuous flow column method. Seven types of insulin microcapsules were respectively injected into the flanks of fasting-diabetic SD rats induced by streptozotocin. The glucose levels and insulin concentrations in the blood were periodically sampled from the tail and assayed by a glucose analyzer and RIA method. Body weights were measured twice per week. The release rate was controllably dependent on the polymer used. The PLA microcapsules could maintain normoglycemia only for five days, whereas the (PLA + 1%EVA) microcapsules exhibited two times the hypoglycemic effect of PLA microcapsules, but (PLA + 1%EVA) microcapsules treated with 4% wax extended the duration of hypoglycemic effects for two weeks. There was no significant effect for insulin-HP-55 microcapsules. The EC microcapsules prolonged the hypoglycemic effect for 15 days, however, the (EC + 1%EVA) microcapsules could maintain the same effect for up to three weeks. The slower the release rate of insulin microcapsules in vitro the longer the hypoglycemic effect of insulin microcapsules in vivo. A close relationship between in vitro release behavior and in vivo hypoglycemic efficacy of insulin microcapsules was obtained.

Animals↗
PubMed1978

[Metabolites of hypoglycemic sulfonylureas in kidney failure. Experience with glibenclamide].

Renal insufficiency is a factor which predisposes to hypoglycemic accidents in subjects treated with hypoglycemic sulfonylureas. Glibenclamide (glyburide) is eliminated from the body mainly by metabolism, with the result that renal insufficiency has little effect on its biotransformation. In order to determine to what extent the retention of the metabolities intervenes in such hypoglycemic accidents, rats with ligatured ureters received intraperitoneal injections of 1 mg/kg glibenclamide or hydroxy-glibenclamide (the main metabolite), or of saline. For each animal there was a control animal which had undergone a simulated operation. For six rats with renal insufficiency, glibenclamide caused hypoglycemia of the same intensity as in the control group but more prolonged. With hydroxy-glibenclamide the glycemia was signficantly lower than in the control group. Hydroxy-glibenclamide has an obvious hypoglycemic activity which represents 1/6 of that of the parent drug, but 50--100 times that of tolbutamide. Its retention contributed to the intensification and prolongation of the hypoglycemic effect of glibenclamide in rats with renal insufficiency.

Acute Kidney Injury↗
PubMed1990

Blood glucose levels stimulating hypoglycemic counterregulation are related to chronic diabetes control.

Intensive insulin therapy is associated with an increased risk of hypoglycemia. To assess the effects of chronic glycemic control on hypoglycemic counterregulation, 21 type I diabetic patients underwent an intravenous insulin infusion of 40 mU/kg/hr for up to 180 min. Five patients had blood glucose levels which fell below 25 mg/dl or significant neurological symptoms ensured. These patients were considered to have inadequate hypoglycemic counterregulation. Of the 16 patients having successfully completed the test, blood glucose levels stabilized at 40 +/- 2 mg/dl after 109 +/- 8 min of insulin infusion, indicating adequate hypoglycemic counterregulation. The levels at which blood glucose stabilized were compared with previous metabolic control as assessed by hemoglobin Alc. A positive correlation (r = 0.57, p = 0.02) was found between the two parameters. It is concluded that (a) long term metabolic diabetes control may affect hypoglycemic counterregulatory mechanisms and (b) intensive insulin therapy may make diabetic patients more vulnerable to hypoglycemia by lowering the effective blood glucose concentration associated with hypoglycemic counterregulation.

Adult↗
PubMedDate not supplied

Catecholamines in the rat brain during hypoglycemic convulsions and coma.

The purpose of the study was to investigate the relation between the catecholamines: noradrenaline and dopamine in the rat brain on one hand and hypoglycemic convulsions and coma on the other. Concentrations of noradrenaline in the hypothalamus, brain stem and cerebral cortex were decreased during hypoglycemic convulsions and were lower during coma than those during convulsions. Dopamine concentration in the striatum was decreased during convulsions and coma. It was shown that the decrease in concentration of catecholamines was a result of hypoglycemia but not of insulin action itself. Clonidine- alpha 2 agonist accelerated occurrence and prolonged duration of hypoglycemic convulsions. Haloperidol-dopamine receptor blocker had no effect on the time of occurrence or duration of convulsions and coma. The results indicate that noradrenaline may exert an inhibitory influence on hypoglycemic convulsions. No evidence has been provided to support involvement of dopamine in the control of hypoglycemic convulsions and coma.

Animals↗
PubMedDate not supplied

[The influence of aging on cerebral energy metabolism following post-hypoglycemic recovery in the rat. Pharmacologic application].

Influence of aging on cerebral energetic metabolism was evaluated during and after severe hypoglycemia in rats respectively 20 (adults), 60 (matures) or 100 (senescents) week-old. Cerebral content of carbohydrates, amino-acids, ammonia, ATP, ADP, AMP, creatine phosphate and creatine was analysed after 20 min insulin induced hypoglycemia and after 20 min hypoglycemic recovery induced by glucose infusion. In the rats of different ages tested, effect of raubasine (0.85 mg X kg-1 i.p. and i.v.), almitrine (2.68 mg X kg-1 i.p. and i.v.) and association almitrine plus raubasine (at the same doses) on post-hypoglycemic recovery was tested. Aging does not affect the cerebral metabolic disorders occurring in severe hypoglycemia, but rather the metabolic changes during the post-hypoglycemic restitution. In fact there is lower restitution of the concentrations of cerebral cortical metabolites in older rats: the concentrations of many amino-acids and adenylate nucleotides remains largely abnormal. Compared with saline treated post-hypoglycemic rats, raubasine decreases by 15 to 20% cerebral glucose and pyruvate contents in "adults" and "matures" rats and by 10 to 15% glutamate content in rat of different ages tested. Almitrine decreases by 20% cerebral glucose concentration in "matures" and "senescent" rats. In this latter group, almitrine decreases lactate and ammonium contents and increases by 23% glutamine level. In rats of all ages that were submitted to 20 min insulin induced hypoglycemia followed by 20 min glucose induced post-hypoglycemic recovery, the association almitrine plus raubasine decreases by 20 to 30% cerebral glucose, pyruvate and lactate contents and decreases by 15% glutamate. In older brains the association almitrine plus raubasine decreases by 50% cerebral content in ammonium and concomitantly induces an equivalent increase in glutamine content. The effect of the combination almitrine plus raubasine is characterized by an increase in rate of metabolic recovery process in all ages tested.

Aging↗
PubMed1998

Cyclosporin A, but not FK 506, protects mitochondria and neurons against hypoglycemic damage and implicates the mitochondrial permeability transition in cell death.

Induction of the mitochondrial permeability transition (MPT) has been implicated in cellular apoptosis and in ischemia-reperfusion injury. During MPT, a channel in the inner mitochondrial membrane, the mitochondrial megachannel, opens and causes isolated mitochondria to swell. MPT and mitochondrial swelling is inhibited by cyclosporin A (CsA), which may also inhibit apoptosis in some cells. Treatment with CsA (50 mg/kg, i.v.) showed a robust reduction of brain damage when administered 30 min before insulin-induced hypoglycemic isoelectricity of 30 min duration. Ultrastructural examination of the dentate gyrus revealed a marked swelling of dendrites and mitochondria during the hypoglycemic insult. In CsA-treated animals, mitochondria resumed a normal and contracted appearance during and after the hypoglycemic insult. Treatment with FK 506 (2 mg/kg, i.v.), a compound with immunosuppressive action similar to that of CsA, was not protective. Studies on the swelling kinetics of isolated mitochondria from the hippocampus showed that CsA, but not FK 506, inhibits calcium ion-induced MPT. We conclude that CsA treatment during hypoglycemic coma inhibits the MPT and reduces damage and that mitochondria and the MPT are likely to be involved in the development of hypoglycemic brain damage in the rat.

Animals↗
PubMed2005

Hypoglycemic effect and chlorogenic acid content in two Cecropia species.

The hypoglycemic effect of methanol leaf extracts from Cecropia obtusifolia and C. peltata was evaluated in healthy mice. A significant decrease (p < 0.05) in plasma glucose levels was recorded 2 and 4 h after a single oral administration of methanol extracts (1 g/kg). This effect was correlated with the chlorogenic acid contents in both species; C. peltata, containing 19.84 +/- 1.64 mg of chlorogenic acid/g of dried leaves produced the highest decrease (D(alpha 2,60) = 20.18, p < 0.05) of plasma glucose levels (52.8%). The extracts of C. obtusifolia from Tabasco and Veracruz, showed similar hypoglycemic effects (33.3% and 35.7%, respectively) and chlorogenic acid contents (Tukey(0.05) = 1.8859) (13.3 +/- 3.2 mg/g and 13.1 +/- 1.6 mg/g, respectively). The hypoglycemic effect produced by different doses (0.1, 0.25, 0.50, 0.75 and 1 g/kg body wt, p.o.) of C. peltata showed a lineal relationship with chlorogenic acid content, reaching an ED(50) = 0.540 g/kg body wt for extract, and an ED(50) = 10.8 mg/kg body wt for chlorogenic acid. These results suggest that C. peltata is a better hypoglycemic agent than C. obtusifolia, and it could be considered for developing a phytomedicinal product to carry out clinical trials.

Animals↗
PubMed2004

Sulfonylurea and non-sulfonylurea hypoglycemic agents: pharmachological properties and tissue selectivity.

ATP-sensitive K+ (K(ATP)) channels play many important roles in cellular functions, including control of membrane excitability of skeletal muscle and neurons, K+ recycling in renal epithelia, cytoprotection in cardiac ischemia, and insulin secretion from pancreatic beta-cells. K(ATP) channels are composed of pore-forming inwardly rectifying potassium channel (Kir6.2 or Kir6.1) subunits and sulfonylurea receptor (SUR1, SUR2A, or SUR2B) subunits. Kir6.2 or Kir6.1 subunits conjoined with a SUR subunit constitute the various tissue-specific K(ATP) channels with distinct pharmacological properties. Both sulfonylureas and non-sulfonylurea hypoglycemic agents are used in treatment of type 2 diabetes mellitus. While the sulfonylurea receptor (SUR) is the target molecule of all of these hypoglycemic agents, the binding sites differ according to the moiety containing in the agent, and alter the pharmachological properties. In addition, chronic exposure of pancreatic beta-cells to the various agents affects the agent-specific sensitivities differently. Here we distinguish differences in pharmacological profile among the various hypoglycemic agents that reflect their chemical composition. We also suggest possible risk in the use of certain hypoglycemic agents in patients with ischemic heart disease.

ATP-Binding Cassette Transporters↗
PubMed2004

Studies on the in vitro and in vivo hypoglycemic activities of some medicinal plants used in treatment of diabetes in Jordanian traditional medicine.

Ferula persica, Paronychia argentea, and Pistacia atlantica are three of the plants widely recommended by the herbalists and used for their hypoglycemic activity in Jordan. Aqueous extracts of these plants were tested in vitro for their alpha amylase inhibitory activity and in vivo for their hypoglycemic activity in normoglycemic and streptozocin-induced hyperglycemic rats. Although the three plants were advocated for their hypoglycemic effects in Jordanian traditional herbal medicine; none of them showed significant hypoglycemic activity compared to the untreated animals. Paronychia argentea and Pistacia atlantica showed significant alpha amylase inhibitory activity while Ferula persica did not demonstrate any alpha amylase inhibitory activity. The main conclusion of this work was the concern over the unjustified claims of the uses of some herbal medicine in Jordan and possibly in other countries.

Animals↗