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 73 records · Page 4Linked to original sources
PubMed2001

Restored hypoglycemic counterregulation is stable in successful pancreas transplant recipients for up to 19 years after transplantation.

BACKGROUND: Pancreas transplantation has been shown to fully restore glucagon response and partially restore epinephrine response to hypoglycemia during the first few years after transplantation in patients with type 1 diabetes. However, prior studies have not examined hypoglycemic counterregulation in any pancreas transplant recipient of more than 6 years' duration. METHODS: To determine whether restoration of hypoglycemic counterregulation is maintained over a prolonged period after transplantation, we studied counterregulatory responses and symptom recognition in two groups of pancreas transplant recipients using a stepped hypoglycemic, hyperinsulinemic clamp. Group 1 consisted of 11 successful transplant recipients of 11 to 19 years' duration (mean+/-SE, 13.9+/-0.7 years). Group 2A consisted of seven successful pancreas transplant recipients of 5 to 11 years' duration (mean+/-SE, 8.7+/-0.9 years) who had been studied approximately 5 years earlier using the same stepped, hypoglycemic clamp technique. RESULTS: Both groups had significant rises in plasma glucagon during the hypoglycemic clamp similar to that seen in short-term recipients and normal controls. Both groups also had significant increases in plasma epinephrine responses similar to that seen in short-term transplant recipients but less than that of normal control subjects. The mean symptom scores of group 1 were significantly less than those of the control group at glucose levels of 60 and 50 mg/dL but not at 40 mg/dL. The mean symptom scores of group 2A were not significantly different than that of control subjects. CONCLUSION: These results indicate that the restoration of hypoglycemic counterregulation by pancreas transplantation remains stable in successful pancreas transplant recipients for up to 19 years after transplantation.

Adult↗
PubMed2004

Effect of insulin hypoglycemic stress on nociceptive responses to mu- and kappa-opioid receptor agonists at LH-surge in female rats.

In a randomized, prospective, controlled and crossover study, the effects of insulin hypoglycemic stress on nociceptive responses to mu- and kappa-opioid receptor directed drugs during steroid-induced preovulatory LH-surge were seen in ovariectomized female rats. Ovariectomized rats were equally distributed in two groups of 10. In group 1 rats, LH-surge was induced by sequential treatment with estradiol benzoate 7.5 micro g/rat s.c. and progesterone 5 mg/rat s.c., whereas in group 2 rats, vehicles of estradiol benzoate and progesterone were given in a sequential manner. A third group consisted of sham-operated rats, which received no treatment. Rats were exposed to insulin-induced hypoglycemic stress 1 h before the peak of LH-surge. Antinociceptive responses of morphine, buprenorphine and pentazocine were observed at peak LH-surge during hypoglycemic stress. Increased nociceptive responses to noxious stimulus and decreased percent maximal possible effect for morphine, buprenorphine and pentazocine at LH-surge were significantly (p < 0.01) reversed during insulin hypoglycemic stress. There was a significant (p < 0.01) decrease in the ED(50) values of morphine, buprenorphine and pentazocine during hypoglycemic stress. The present study indicates that insulin hypoglycemic stress is responsible for increased antinociceptive activities of morphine, buprenorphine and pentazocine and decreased sensitivity to noxious stimulus in ovariectomized rats with or without steroid-induced LH-surge.

Analgesics, Opioid↗
PubMed1989

Effects of brief exposure to insulin-induced hypoglycemic serum during organogenesis in rat embryo culture.

We have previously shown that long-term exposure to medium containing insulin-induced hypoglycemic serum during the early phase of organogenesis can adversely affect embryonic development in rat embryo culture and that these effects were mediated through the interruption of glycolytic flux that constituted the principal pathway at this embryonic stage. Further experiments were performed to examine whether brief exposure to the hypoglycemic medium during critical developmental periods would have adverse effects on embryogenesis during embryo culture not only in normal but also in high glucose concentrations. Rat embryos in the early head-fold stage (9.5 days gestation) were grown in vitro for 48 h until neural tube closure occurred; dysmorphogenic lesions were not elicited in either the basal culture medium containing 6.6 mM glucose (control medium) or the hyperglycemic medium supplemented with glucose at a concentration of 33.3 mM. Hypoglycemic mediums (2.2-2.5 mM glucose) were prepared from the serum of rats given insulin intraperitoneally. Postimplantation embryos (in early neural tube formation) were briefly exposed (1 h) to hypoglycemic medium on day 10.3 of gestation during the basal culture. After exposure to the hypoglycemic medium for 1 h during culture in the control medium, embryos showed minor growth retardation and dysmorphogenic lesions (7.1% open neural pores). Exposure to the hypoglycemic medium for 1 h during culture in hyperglycemic medium suplemented with a subteratogenic concentration of glucose (33.3 mM) resulted in greater growth retardation and increased occurrence of dysmorphogenic lesions (17.3% open neural pores).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Hypoglycemic detection does not occur in the hepatic artery or liver: findings consistent with a portal vein glucosensor locus.

Our laboratory has previously demonstrated that hypoglycemic detection occurs in the portal vein, not the liver. To ascertain whether hypoglycemic detection may also occur in the hepatic artery, normoglycemia was established across the liver via a localized hepatic artery glucose infusion. Male mongrel dogs (n = 7) were infused with insulin (5.0 mU x kg(-1) x min(-1)) via the jugular vein to induce systemic hypoglycemia. Animals participated in two hyperinsulinemic-hypoglycemic clamp experiments distinguished by the site of glucose infusion. During the liver irrigation protocol, glucose was infused via the hepatic artery (HA protocol) to maintain liver normoglycemia as systemic glucose concentrations were systematically lowered over 260 min (nadir = 2.2 +/- 0.01 mmol/l). During control experiments, glucose was infused peripherally (PER protocol) to control reductions in blood glucose. Arterial glucose concentrations were not significantly different at any time between the two protocols (P = 0.73). Hepatic artery and liver glucose concentrations were significantly elevated in the HA versus PER protocol throughout the duration of the progressive hyperinsulinemic-hypoglycemic clamp. During the PER protocol, epinephrine and norepinephrine concentrations increased significantly above basal values (0.53 +/- 0.06 and 0.85 +/- 0.2 nmol/l, respectively) to plateaus of 4.4 +/- 0.86 (P = 0.0001) and 3.6 +/- 0.69 nmol/l (P = 0.001), respectively. There were no significant differences between the two protocols in the epinephrine (P = 0.81) and the norepinephrine (P = 0.68) response to hypoglycemia. The current findings indicate that glucosensors important to hypoglycemic detection do not reside in the hepatic artery. Furthermore, these data confirm our previous findings that glucosensors important to hypoglycemic detection are not present in the liver, but are in fact localized to the portal vein.

Animals↗
PubMed1992

IGF-I and IGF-II protect cultured hippocampal and septal neurons against calcium-mediated hypoglycemic damage.

Insulin and insulin-like growth factors I and II (IGF-I and IGF-II) have recently been shown to have biological activity in central neurons, but their normal functions and mechanisms of action in the brain are unknown. Since central neurons are particularly vulnerable to hypoglycemia that results from ischemia or other insults, we tested the hypothesis that growth factors can protect central neurons against hypoglycemic damage in vitro. IGF-I and IGF-II (3-100 ng/ml) each prevented glucose deprivation-induced neuronal damage in a dose-dependent manner in rat hippocampal and septal cell cultures. High concentrations of insulin (greater than 1 microgram/ml) also protected neurons against hypoglycemic damage. Epidermal growth factor did not protect against hypoglycemic damage. Both IGFs and insulin were effective when administered 24 hr before or immediately following the onset of glucose deprivation. Direct measurements of intraneuronal calcium levels and manipulations of calcium influx demonstrated that calcium influx and sustained elevations in intraneuronal calcium levels mediated the hypoglycemic damage. IGF-I and IGF-II each prevented the hypoglycemia-induced elevations of intraneuronal free calcium. Studies with excitatory amino acid receptor antagonists and calcium channel blockers indicated that NMDA receptors did, and L-type calcium channels did not, play a major role in hypoglycemic damage. Taken together, these findings indicate that IGFs can stabilize neuronal calcium homeostasis and thereby protect against hypoglycemic damage.

Animals↗
PubMed1991

Inhibitory effect of cyclosporine A on the activity of oral hypoglycemic agents in rats.

Diabetic patients often have a kidney or pancreas allograft requiring cyclosporine A (CsA) to prevent transplant rejection. These patients usually take p.o. hypoglycemic agents to control their diabetes. Because of the reported adverse effects of CsA on glucose metabolism as well as its potential use in Type II diabetics, we were interested in evaluating the in vivo effect of CsA on the activity of p.o. hypoglycemic agents. We also wanted to determine if tolbutamide produced any adverse effects on the pharmacokinetics of CsA. Male, Holtzman rats were administered CsA (p.o.) followed 1 hr later with the hypoglycemic agent. Two hours later, blood samples were obtained to determine blood glucose levels. Animals treated with CsA alone produced a significant hyperglycemia. The hypoglycemic effects produced by tolbutamide and glyburide were inhibited in animals treated concomitantly with CsA. This inhibitory effect was not observed during the first 3 hr of CsA-treatment, could not be overcome by increasing the dose of the hypoglycemic agent and occurred using small doses. CsA did not, however, interfere with the activity of exogenous NPH insulin. Tolbutamide was found to have no effect on the acute pharmacokinetics of CsA. The distribution of CsA was similar to controls in all tissues studied except the liver in which CsA levels were less in tolbutamide-treated animals. These studies demonstrate that CsA interferes with the effects of p.o. hypoglycemic agents and, therefore, blood glucose levels should be monitored closely in Type II diabetic patients taking combinations of these drugs.

Administration, Oral↗
PubMed2003

A cohort study of the incidence of serious acute liver injury in diabetic patients treated with hypoglycemic agents.

BACKGROUND: The incidence of acute liver failure or serious liver injury in diabetic patients is needed to evaluate the safety of hypoglycemic drug therapy. METHODS: We conducted a retrospective cohort study of 5 health maintenance organizations. Study patients were 171,264 health plan members 19 years or older when they received oral hypoglycemic drugs or insulin between April 1, 1997, and June 30, 1999. We searched for hospital discharge diagnoses and procedures potentially indicative of acute liver injury and reviewed the full-text medical records. Acute liver failure was defined as acute liver disease and (1) hepatic encephalopathy, (2) prothrombin time prolongation greater than 3 seconds or international normalized ratio greater than 1.5, and (3) a total bilirubin level greater than 3.0 mg/dL (>51 micro mol/L). Acute liver injury was diagnosed in individuals who did not meet 1 or more of the criteria for acute liver failure but had alanine transaminase or aspartate transaminase levels greater than 500 U/L. RESULTS: We identified 35 cases of acute liver failure or injury not clearly attributable to a known cause other than use of hypoglycemic agents. The age- and sex-standardized incidence per 1000 person-years was 0.15 for insulin users, 0.08 for sulfonylurea users, 0.12 for metformin users, and 0.10 for troglitazone users. The incidence was higher (on the order of 0.3 per 1000) during the first 6 months of exposure to all hypoglycemic agents. CONCLUSIONS: Acute liver failure or injury not clearly attributable to other known causes occurred on the order of 1 per 10,000 person-years among diabetic patients treated with oral hypoglycemic drugs or insulin.

Acute Disease↗
PubMed2001

Hypoglycemic neuropathy.

Hypoglycemia is a relatively common condition primarily affecting diabetic patients treated with insulin or other hypoglycemic drugs and insulinoma patients. Clinical experience and experimental studies show that hypoglycemia may cause alterations both in the central (CNS) and the peripheral (PNS) nervous system. Hypoglycemic effects on the CNS include various symptoms such as irritability and lack of concentration, disruption of cognitive functions, convulsions and unconsciousness. As for pathology, a loss of neurons has been noted, being more obvious in the cerebral cortex and the hippocampus than in the brain stem, cerebellum and spinal cord. Myelin damage and glial changes have also been observed in the CNS. The development of pathological changes in the brain has mainly been studied on autopsy material from patients who died in insulin coma and in animals exposed to a severe hypoglycemia and showing an isoelectric electroencephalogram. It has been suggested that hypoglycemic loss of neurons in the brain is related to excititoxic actions of aspartate on N-methyl-D-aspartate receptors. With respect to the PNS, scattered clinical observations in humans and experimental studies in animals show that hypoglycemia causes a distal axonopathy including both degenerative and regenerative events. In this respect, motor axons seem to be more vulnerable than sensory axons. Animal experiments show that a peripheral neuropathy may develop even in cases with a mild hypoglycemia compatible with a generally normal behavior. The cellular mechanisms behind the development of hypoglycemic PNS alterations are unknown. To elucidate the pathophysiology of hypoglycemic neuropathy more basic research is needed.

Diabetic Neuropathies↗
PubMed2005

Potential hypoglycemic effects of Chlorella in streptozotocin-induced diabetic mice.

Chlorella, a type of unicellular fresh water algae, has been a popular foodstuff in Japan and Taiwan. Chlorella has been shown to produce hypoglycemic effects in alloxan-induced diabetic animals. However, there are no other reports of the effects of this substance in other diabetic animal models. Here we have used streptozocin (STZ)-induced diabetic mice to study the thypoglycemic effects of Chlorella. Diabetes was induced in ICR strain mice by the i.p. injection of STZ. Vehicle-treated ICR mice were used as normal control animals and glibenclamide was used as a positive drug control. The effects of Chlorella on basal blood glucose, exogenous insulin sensitivity test and plasma insulin levels were measured. In normal mice Chlorella produced a transient hypoglycemic effect at 90 min after acute administration; whereas glibenclamide produced a more sustained hypoglycemic effect between 90 min and 180 min after acute administration. Chlorella did not affect the basal blood glucose level in STZ mice. However, Chlorella enhanced and prolonged the hypoglycemic effects of injected insulin in STZ mice for a further 60 min compared to the normal vehicle-treated group. Plasma insulin levels were increased in normal mice after treatment with glibenclamide, whereas Chlorella had no such effect. The current results indicate that Chlorella enhances the hypoglycemic effects of exogenous insulin at a dose which does not produce hypoglycemia in STZ mice, suggesting that insulin sensitivity is increased in these mice.

Administration, Oral↗
PubMed1997

Oral hypoglycemic agents for noninsulin-dependent diabetes mellitus in the cat.

The use of oral hypoglycemic agents for the treatment of noninsulin-dependent diabetes mellitus (NIDDM) is still in its infancy. The purpose of this article is to summarize the current knowledge regarding the use of oral hypoglycemic agents in cats. Oral hypoglycemic therapy is more successful when the veterinarian is aware of the mechanism of action of the drug, as well as its dosage, side effects, and drug interactions. A short section on combining insulin with oral hypoglycemics and monitoring therapy with oral hypoglycemic agents is also included.

Administration, Oral↗
PubMed2004

Oral hypoglycemic agents in pregnancy.

UNLABELLED: Pregnancies in diabetic women are associated with increased risk of spontaneous abortion, congenital malformations, preeclampsia, preterm labor, macrosomia, shoulder dystocia, and cesarean section. Advances in antepartum cares and strict adherence to dietary and insulin regimens have been shown to significantly reduce the rate of maternal morbidity as well as perinatal morbidity and mortality. Historically, reports of potential fetal teratogenicity and hypoglycemic effects on the fetus contraindicated the use of oral hypoglycemic agents in pregnancies complicated with either type II diabetes mellitus (DM) or gestational diabetes mellitus (GDM). Recently, physicians increasingly prescribe newer generations of oral hypoglycemic agents to treat GDM and type II DM to pregnant patients. This review addresses the safety, current recommendations, and controversies surrounding use of the available oral hypoglycemic agents during pregnancy. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians LEARNING OBJECTIVES: After completion of this article, the reader should be able to describe the mechanisms of actions of the various oral hypoglycemic agents, to list the known side effects of these agents, and to summarize the data on the use of these agents during pregnancy.

Administration, Oral↗
PubMed1995

Normalization of impaired glucose tolerance by the short-acting hypoglycemic agent calcium (2S)-2-benzyl-3-(cis-hexahydro-2-isoindolinylcarbonyl)propionate dihydrate (KAD-1229) in non-insulin-dependent diabetes mellitus rats.

We have investigated the hypoglycemic effects of the newly synthesized short-acting nonsulphonylurea hypoglycemic agent calcium (2S)-2-benzyl-3-(cis-hexahydro-2-isoindolinylcarbonyl)-propionate dihydrate (KAD-1229) in non-insulin-dependent diabetes mellitus (NIDDM) rats. NIDDM rats that were given a neonatal injection of 60 mg/kg streptozotocin showed a dose-dependent but attenuated response to oral administration of KAD-1229 and gliclazide, and their impaired glucose tolerance was improved but not normalized. We next produced, using a neonatal injection of 30 mg/kg streptozotocin, a mild type of NIDDM rat with less impaired glucose tolerance. These rats responded well to these insulinotropic hypoglycemic agents. Their impaired glucose and meal tolerance were completely normalized by oral administration of 3 mg/kg KAD-1229. The efficacy of KAD-1229 in this NIDDM rat model 1-3 h after oral glucose administration was comparable with similar doses of gliclazide, despite its shorter hypoglycemic action (compared with gliclazide), in fasting normal rats. In meal tolerance tests (20 kcal/kg; 1 cal = 4.2 J), KAD-1229 reduced abnormally enhanced plasma glucose levels 1-3 h after administration. This effect disappeared by 5 h. In contrast, gliclazide showed sustained hypoglycemic effects until 5 h after oral administration, with a lower postprandial (0.5-1 h) effect. These data indicated that the rapid- and short-acting efficacy of KAD-1229 would be beneficial and sufficient to control postprandial plasma glucose in NIDDM rats.

Animals↗
PubMed1999

Type 1 diabetes mellitus in early childhood: glycemic control and associated risk of hypoglycemic reactions.

OBJECTIVE: To assess the level of glycemic control and to determine whether more normal glycemic control, as measured by glycosylated hemoglobin, leads to frequent hypoglycemic episodes in young patients with type 1 diabetes mellitus. MATERIAL AND METHODS: We undertook a retrospective review of the medical records of 59 children with type 1 diabetes diagnosed at age 9 years or younger, who underwent follow-up at our institution for at least 2 years. For each follow-up, insulin requirements, levels of glycosylated hemoglobin, and frequency of hypoglycemic reactions were analyzed for three age-groups--0 to 2 years, 2 to 5 years, and 5 to 9 years old. RESULTS: The mean glycosylated hemoglobin for the first 2 years after diagnosis of type 1 diabetes was higher in children 0 to 2 years old in comparison with the other age-groups. This increased glycosylated hemoglobin occurred despite increased administration of insulin, expressed in units per kilogram daily, to these children (P < 0.05). Severe hypoglycemic reactions were more common in infants (55%) and children between 2 and 5 years old (45%) than in children from 5 to 9 years old (13%). In all age-groups, the mean glycosylated hemoglobin value closest to a hypoglycemic event and the mean glycosylated hemoglobin value for the 2-year study period were similar but were both less than 8% (the standard established by the Diabetes Control and Complications Trial). Most reactions had no clear cause in the youngest age-group, whereas a specific reason could usually be determined in children 2 to 5 years old. CONCLUSION: Tight glycemic control is achievable in young patients with type 1 diabetes mellitus. Such tight control, however, may lead to an increase in the frequency of severe hypoglycemic reactions in this patient population. Our data support the guideline that children younger than 5 years should have a higher goal for premeal plasma glucose levels.

Age Factors↗
PubMed2004

Hypoglycemic efficacy of chitosan-coated insulin liposomes after oral administration in mice.

AIM: To evaluate the hypoglycemic efficacy of insulin liposomes coated by chitosan with different molecular weights and concentrations after oral administration in mice. METHODS: Insulin-liposomes were prepared by reversed-phase evaporation. Chitosan coating was carried out by incubation of the liposomal suspensions with the chitosan solution. The hypoglycemic efficacies of chitosan-coated insulin liposomes were investigated by monitoring the blood glucose level using the glucose oxidase method after oral administration to healthy mice. RESULTS: In all the insulin liposomes, the insulin liposomes coated by 0.2% chitosan (Mr 1000 kDa) showed a better hypoglycemic efficacy as compared with the other liposomes coated by chitosan. The minimum blood glucose level was 15.1%+/-6.0 % of the initial (n=6). The hypoglycemic efficacy lasted for 4 h after oral administration to mice. CONCLUSION: Chitosan-coated liposomes could reduce tryptic digestion on insulin, and enhance enteral absorption of insulin. The molecular weights and concentrations of chitosan had significant effects on hypoglycemic efficacy of chitosan-coated insulin liposomes after oral administration to healthy mice.

Administration, Oral↗
PubMed2005

Enhancing dissolution, serum concentrations and hypoglycemic effect of glibenclamide using solvent deposition technique.

PURPOSE: Glibenclamide is practically insoluble in water and its GI absorption is limited by its dissolution rate. Therefore, to enhance the drug dissolution, serum concentrations and its hypoglycemic effects, it was formulated as solid dispersions and evaluated the relevant in vitro and in vivo parameters. METHODS: The drug solid dispersions were prepared by solvent deposition technique using microcrystalline cellulose as the carrier in different ratios and their dissolution rates were compared to those of pure drug and its physical mixture with carrier. Drug serum concentrations and hypoglycemic effects in rabbits of pure drug, a physical mixture and the corresponding solid dispersion were investigated. In order to elucidate the observed in vitro and in vivo differences, IR spectroscopy and x-ray diffraction patterns of the formulations were studied. RESULTS: The solid dispersion with the drug to carrier ratio of 1:19 showed the highest dissolution rate with the dissolution efficiency (DE) of 44.42 in comparison to pure drug (DE = 3.82), physical mixture (DE = 4.91) and other solid dispersions (DE between 13.85-39.94) and also produced higher drug serum concentrations (more than 4 times at 6th hour post dose) as well as enhanced hypoglycemic effects relative to pure drug and its corresponding physical mixture. CONCLUSIONS: Solvent deposition technique was proved an effective tool of increasing dissolution probably due to enhanced wettability and reduced drug particle size, which in turn led to enhance drug serum concentrations and its hypoglycemic effects. Strong quantitative correlations were established between dissolution parameter and parameters related to serum concentrations as well as hypoglycemic effects.

Animals↗
PubMed1994

Novel rapid- and short-acting hypoglycemic agent, a calcium(2s)-2-benzyl-3-(cis-hexahydro-2-isoindolinylcarbonyl) propionate (KAD-1229) that acts on the sulfonylurea receptor: comparison of effects between KAD-1229 and gliclazide.

Calcium(2s)-2-benzyl-3-(cis-hexahydro-2-isoindolinylcarbonyl) propionate dihydrate (KAD-1229) was found to have potent hypoglycemic effects. This study was designed to elucidate its mechanisms by comparing its action with those of the antidiabetic hypoglycemic agents known as sulfonylureas in vivo and in vitro. In fasted beagles, oral administration of 0.1 to 3.0 mg/kg of KAD-1229 induced dose-dependent and significant reductions of plasma glucose levels with 43.4% maximum reduction at 1 hr, and the significant hypoglycemic effects largely disappeared within 2 hr after oral administration; 1.0 to 10 mg/kg of gliclazide also induced dose-dependent and significant reductions of plasma glucose with 44.2% maximum reduction at 3 hr, and the hypoglycemic effects continued for over 7 hr. One and 3.0 mg/kg of KAD-1229 increased plasma insulin levels, with the peak levels at 30 min, whereas 3.0 and 10 mg/kg of gliclazide increased it with the peak levels at 1 to 2 hr after dosing. Similar rapid and short-acting hypoglycemic effects of KAD-1229 were observed in rats. This compound stimulated insulin release from isolated mouse islets at a concentration from 3 x 10(-7) M to 10(-5) M. KAD-1229 stimulated insulin release from hamster's insulin-oma cell line, HIT T15 cells, at a concentration from 10(-8) M to 10(-5) M and inhibited 86Rb+ efflux from these cells with IC50 of 8.4 x 10(-9) M. It also inhibited [3H]glibenclamide binding to microsomes from HIT T15 cells (Ki = 1.3 x 10(-8) M).(ABSTRACT TRUNCATED AT 250 WORDS)

ATP-Binding Cassette Transporters↗
PubMed1993

[Drug consumption in diabetes mellitus (III). Trends of hypoglycemic agents use and consumption in Tarragona, Catalonia, and Spain (1988- 1991). Group for the Study of Diabetes in Tarragona].

BACKGROUND: To analyze the evolution of the use of drugs in diabetes, the consumption of hypoglycemic medication in the province of Tarragona, the autonomic community of Catalonia and Spain as a whole, was studied. A qualitative evaluation of the tendencies of prescription, as an indirect index of quality in the health care to diabetics was performed. METHODS: The sales of oral hypoglycemic medication (OH) and insulin (INS) were accounted for in the study environment between 1988-1991. To make consumption uniform a standardized unit of measure was used with defined daily doses (DDD)/1,000 inhabitants/day (Drug Utilization Research Group) of the different groups of drugs. Total consumption was obtained by a primary data source (Intercontinental Medical Statistics), and periodically compared with a secondary source (registry of public prescriptions within Tarragona). RESULTS: A progressive increase in the consumption of hypoglycemic drugs was observed: 16.1 to 21.2 DDD/1,000 inhabitants/day (31%) in Spain; 17.7 to 19.8 (12%) in Catalonia and 19 to 23 (21%) in Tarragona. The increase in consumption of INS in Tarragona (43%) was greater than that of OH (12%). In Catalonia, it was much greater (INS: 23%, OH: 7%) and was parallel in Spain (36% and 30%, respectively). The OH/INS index decreased in Catalonia and Tarragona (1.3 and 1.9 in 1991) and remained practically constant (2.3-2.4) in Spain. A global decrease was produced in the consumption of slow insulins with a significant increase in intermediate, premixed and fast insulins. A growing increase in glibenclamide much greater than the remaining sulphonylureas was seen, in addition there was a persistent and low use (less than 1 DDD/100 inhabitants/day) of biguanides. Significative variations of medication consumption were registered according to the territory analyzed. CONCLUSIONS: From 1988 to 1991 there has been an increase in the use of hypoglycemic drugs. The use of oral hypoglycemics has remained constant in relation to insulins in Spain and in Catalonia and, more so in Tarragona, there is a progressive inclination to the use of insulin. The evolution of consumption suggests important asymmetry in the quality of health care and denotes progression in the global educative offer to diabetics.

Diabetes Mellitus↗
PubMed1975

Hypoglycemic conditioned reflex in rats: preliminary study of its mechanism.

It was found that a nervous mechanism is involved in eliciting a hypoglycemic response in rats. A conditioned reflex was established after a series of reinforcements in which an insulin injection (unconditioned stimulus) was associated with the sound of a bell (conditioning stimulus). The hypoglycemic conditioned response was statistically similar to that of insulin. The latency of the beginning of the hypoglycemic response to insulin was between 4 and 6 min. The latency of the conditioned hypoglycemic response to the conditioning stimulus was about 1 min. Blood extracted from a conditioned rat during the test of conditioning produced a hypoglycemic effect when injected into a nonconditioned receptor rat.

Animals↗