Fall In Blood Sugar Research Articles

Arrhythmias and diabetes: heart block, ventricular arrhythmias, and death

Arrhythmias and diabetes: heart block, ventricular arrhythmias, and death

Evaluation of Hypoglycemic potential of Moringa oleifera bark extracts on normal and Alloxanized diabetic rats

Diabetes Mellitus is a leading community health agony. Although steady new drug evolution to care intended for diabetes, herbal remedy stay a prospective add-on remedy to maintain glucose level in the body. Moringa oleifera (Moringaceae) has been conventionally used to deal with numerous diseases as the anti-oxidant properties it reports. The effect M. oleifera stem bark extracts against diabetes alloxanized diabetic rats were employed in this research. Bark of M. oleifera stem was used. Male Wistar albino rats (150–200g) were employed. Blood samples were accumulated by retro-orbital plexus puncture method and blood glucose of all animals was examined by means of an electronic glucometer. Diabetes commences due to Alloxan during its capability to demolish the insulin-generating beta cells of the pancreas. Three weeks observations indicate drop in blood glucose levels as in Alloxan + glibenclamide (10mg/kg) used as standard from 295mg/dl to 149mg/dl. Alloxan + Methanolic extract of M. oleifera (100mg/kg) from 294 mg/dl to 237mg/dl. Alloxan + Methanolic extract of M. oleifera (200mg/kg) from 295mg/dl to 232mg/dl. Alloxan + Methanolic extract of M. oleifera (400 mg/kg) from 290mg/dl to 229mg/dl. Three weeks of daily treatment of extract of M. oleifera led to a dose dependent fall in blood sugar in three weeks for methanolic extract of M. oleifera. The current research concludes that extracts of M. oleifera bark is able to demonstrate drop in blood glucose level in normal and alloxan treated rats.

From Insulin and Insulin-Like Activity to the Insulin Superfamily of Growth-Promoting Peptides: A 20th-Century Odyssey

In 1941, Gellhorn reported that administration of human blood to hypophysectomized/adrenodemedullated rats caused a fall in blood sugar. This was among the early demonstrations that human blood possesses glucose-lowering or insulin-like activity (ILA). Gellhorn assumed he had detected only insulin. During the 1960s, however, it became evident that plasma ILA contained at least two components: one, suppressible ILA (SILA), was inactivated by anti-insulin antibody and was therefore considered to be indistinguishable from pancreatic insulin; the other, nonsuppressible ILA (NSILA), was unaffected by anti-insulin antibody. Subsequent work resolved NSILA into insulin-like growth factors I and II (IGF-I and IGF-II), two 7.5 kilodalton peptides with potent mitogenic properties; established their identity with the somatomedins; and investigated both their therapeutic potential and role in the pathogenesis of neoplastic and other human diseases. Insulin and the IGFs exhibit striking homologies in amino acid composition and some degree of overlap in their signaling pathways and actions. Moreover, insulin-like proteins have been identified not only in all vertebrate classes but also in molluscs, insects, and worms. These observations are the basis for the hypothesis that the genes encoding vertebrate insulins and IGFs and invertebrate insulin-like molecules evolved from a common ancestral gene, and for the concept of an insulin superfamily of growth-promoting peptides.

Hypoglycemic Properties of Viscum album (Mistletoe) in Alloxan-induced Diabetic Animals

The aqueous leaf extract of Viscum album Stapf (Loranthaceae) given i.p. produced a dose-dependent fall in blood sugar. Doses of 200 mg/kg and 400 mg/kg body weight produced significant (p < 0.05) lowering of blood sugar in fasted normal white albino rats and alloxanized rabbits respectively. The fasting blood sugar, measured in milligram per 100ml (mg%), in normoglycemic rats was reduced by 30.06% while in alloxanized rabbits, the blood sugar was reduced from mean value of 650 ± 7.2mg % at zero hour to 87 ± 8.2mg% at 4h. The hypoglycemic effects were compared with those of tolbutamide. Acute toxicity studies of the extract in mice gave LD 50 value of 4.18 ± 0.96 g/kg body weight when given i.p. The mechanism underlying the observed hypoglycemic effect of V. album extract is not fully understood but may be related to enhancement in peripheral utilization of glucose and increase in insulin secretion.

Hypoglycaemic properties of the aqueous root extract of Morinda lucida (Benth) (Rubiaceae). Studies in the mouse

AbstractThe aqueous root extract of Morinda lucida (Rubiaceae) Benth, exhibited potent hypoglycaemic effects in both normoglycemic and alloxan‐induced diabetic mice by oral administration. This effect was dose‐dependent and more potent than that observed with chlorpropamide (1‐(p‐chlorobenzene‐sulphanyl)‐3‐propylurea). In the normoglycaemic mice, the extract (140 mg/kg body weight) produced a fall in blood sugar of 32% + 1% while at 280 mg/kg body weight there was a 52% + 2% fall over the same time interval.In alloxan‐induced diabetic mice, the reaction time of the extract was longer with a single dose of the extract producing a significant hypoglycaemic effect 4 h after administration. In diabetic mice, a dose of 140 mg/kg body weight of the plant extract caused a fall in blood sugar of 51% + 1% while a dose of 280 mg/kg produced a fall of 60% + 2%.

Antidiabetic and adaptogenic properties of Momordica charantia extract: An experimental and clinical evaluation

AbstractThe hypoglycaemic properties of Mormodica charantia (bitter gourd) water extract was tested on alloxan diabetic rats experimentally. A fall of blood sugar after 3 week's treatment with aqueous extract of fruits of the herb was found to be significant (p&lt;0.01). The aqueous extract of fruit was more effective in diabetes (fall of blood sugar 54% after 3 week's therapy) than the powder of the dried fruit (fall 25% nonsignificant). Hypoglycaemic effects in diabetic patients were found to be highly significant (p&lt;0.01) at the end of the trial but were cumulative and gradual, unlike that produced by insulin. Adaptogenic properties are indicated by the delay in the appearance of cataracts, the secondary complications of diabetes and relief in neurological and other common symptoms even before the hypoglycaemia occurred.

Blood sugar lowering effect of Vernonia amygdalina Del, in an experimental rabbit model

AbstractThe aqueous leaf extract of Vernonia amygdalina, Del, (Compositae) given i.p. produced a dose‐related fall in blood sugar. A dose of 80 mg/kg body weight of adult rabbit produced a maximum lowering of blood sugar in both fasted normal and alloxanized rabbits. The fasting blood sugar in normoglycaemic rabbits was reduced from 96 mg% to 48 mg% in 4 h. In alloxanized rabbits, the blood sugar was reduced from the mean value of 520 mg% to 300 mg% in 8 h. The hypoglycaemic effects were compared with those of tolbutamide. Acute toxicity studies of the extract in mice gave LD50 value of 1122 mg/kg body weight when given i.p. The blood sugar lowering effect of Vernonia amygdalina extract may involve a mechanism not related to insulin secretion.

Protein metabolism during treatment of chest infection in patients with cystic fibrosis

Six cystic fibrosis patients with pulmonary exacerbations were studied to determine the effect of antibiotic treatment on protein nutritional status. Indirect calorimetry, nitrogen balance, protein turnover, urinary 3-methylhistidine, plasma albumin, prealbumin transferrin, and cortisol were measured before and after treatment. N loss averaged 16 and 17% on each balance. N in the sputum was up to 4.5% of absorbed N intake. At the peak of infection, protein synthesis, degradation, and urinary 3-methylhistidine were significantly higher than during recovery (31%, 28%, and 60%, respectively). On recovery a significant fall in blood sugar, albumin, morning cortisol and sputum N and a rise in prealbumin was found. Basal metabolic rate and N balance did not change. For patients in the fed state, active infection is associated with higher rates of protein synthesis and degradation. Antimicrobial treatment alters protein dynamics but does not alter measured N balance or the difference between measured protein synthesis and breakdown.

Low-dose insulin treatment of hyperosmolar diabetic coma

The effect of low-dose hourly i.m. injections of insulin has been studied in the treatment of 17 episodes of hyperosmolar non-ketoacidotic diabetic coma compared with 26 episode of hyperosmolar ketoacidosis occurring in patients over 40 years of age. The fall in blood sugar was satisfactory in the majority of episodes of both types of coma and there was no evidence that patients with hyperosmolar non-ketoacidotic coma were more sensitive to insulin. The excess mortality in the non-ketotic group (47%) compared with the ketoacidotic group (16%) was not due to uncontrolled diabetes.

β-BLOCKERS and BLOOD SUGARS

Summary Catecholamines mediate sympathetic activity throughout the body and, since carbohydrate metabolism is under sympathetic control they influence the availability of glucose for utilization as energy. They achieve this by modifying the response to a raised blood sugar by either suppressing insulin release, an a-receptor stimulant effect, or by promoting insulin release, probably a β2 stimulant effect. When the blood sugar falls, catecholamines initiate metabolic processes which increase blood glucose and restore it to normal. This is also thought to be a β2-receptor stimulant effect. It would therefore be expected that drugs which blocked β-adrenoreceptors would interfere with both the insulin release which occurs during hyperglycaemia and the glycogenosis and gluconeogenesis which occur in response to a fall in blood sugar. Both of these actions have been demonstrated in acute studies usually in volunteers. The clinical relevance of these effects remains to be determined though some guidelines can be suggested on the basis of data currently available, and are given at the end of the paper.

Comparison of the changes in plasma human growth hormone (HGH) and immuno-reactive glucagon (IRG) after intravenous and subcutaneous injection of glucagon.

Ten healthy male volunteers were studied to compare the effectiveness of intravenous and subcutaneous injections of 1 mg of glucagon on HG secretion. Plasma HGH level rose to a peak of 6 ng/ml or greater 120 minutes after the subcutaneous injection of glucagon (sc glucagon) in all subjects, whereas the intravenous injection of glucagon (iv glucagon) caused comparable increments in plasma HGH in only six out of ten subjects. Furthermore, in comparison to those in sc glucagon the periods required to show maximum responses were less consistent in iv glucagon. Plasma IRG levels reached a peak of 102.4+/-22.6 ng/ml at two minutes following iv glucagon, and a peak of 3.33+/-1.08 ng/ml at 15 minutes following sc glucagon. These fell to initial levels at 60 minutes and at 180 minutes, respectively. There was no definite correlation either between the magnitudes of changes in plasma IRG and HGH levels or between the velocities of decrement in blood sugar and HGH responsiveness. Judging from its simplicity and reproducibility it may be concluded that sc glucagon is more suitable for a clinical provocative test of HGH release than is iv glucagon. In regards to the mechanism of glucagon-induced HGH release, neither glucagon per se nor the fall of blood sugar after hyperglycemia was assumed to play any major role. The sustained elevation of plasma IRG for a certain period might be responsible for the glucagon-induced HGH release.

Adrenal function in the carcinoid syndrome: Effects of the serotonin antagonist cyproheptadine

Results of evaluations of adrenal function in 11 patients with carcinoid tumors are presented. Nine patients had tumors that made and secreted serotonin resulting in elevated 5-hydroxyindoleacetic acid (5-HIAA), elevated serum serotonin, and the carcinoid syndrome; while two patients had tumors that did not make serotonin and that did not cause elevated 5-HIAA excretion or elevated serum serotonin. All of the patients had normal 24-hr 17-hydroxycorticosteroid excretion. In the group of patients with tumors actively secreting serotonin, the correlation between 17-hydroxycorticosteroid and 5-HIAA excretion (r = 0.44) was not significant. Six of these patients pretreated with cyproheptadine (CYPRO), a serotonin antagonist, experienced a 36% mean decrease in 17-hydroxycorticosteroid excretion, a finding that was not present when three of them were treated with triprolidine (TPRO), an antihistamine. Serum cortisol at 8 a.m. was normal in all patients except two whose values were mildly elevated, and these two patients showed evidence of suppression of ACTH secretion secondary to dexamethasone treatment. There was a significant positive correlation between serum-cortisol concentrations and 5-HIAA excretions (r = 0.73, p < .05). Normal diurnal variation was present in six patients in whom it was determined. The serum-cortisol response to insulin-induced hypoglycemia in six patients who had carcinoid tumors actively secreting serotonin was not statistically different from that of 12 normal volunteers. Comparisons between these two groups were difficult because the carcinoid patients' fall in blood sugar was 50%, whereas that of the control group was to 38% of the fasting glucose concentration. Six patients with actively secreting carcinoid tumors responded to standard metyrapone testing with a mean increment of 22.8 ± 2.5 mg/day in 17-hydroxycorticosteroids. This response was statistically different from the increment of 13.8 ± 5.3 mg/day in 17-hydroxycorticosteroid excretion found in 34 agematched hospitalized control patients. When the tests were repeated in four of the patients with carcinoid tumors after pretreatment with CYPRO, the increment in 17-hydroxycorticosteroid excretion was reduced well below the mean increment of the control group. Peak serum 11-deoxycortisol (Compound S) values during the test were also reduced. This decrease in the metyrapone response after CYPRO pretreatment was not due to changed peripheral cortisol metabolism, altered adrenal responsiveness to ACTH, interference with recovery of 17-hydroxysteroids by the Porter-Silber reaction, altered metyrapone metabolism, or reduced renal clearance of Compound S. These changes in adrenal response to metyrapone were not seen when the patients were pretreated with TPRO. Our data suggest that the alterations in adrenal function in our patients may be related to elevated serum serotonin. If CYPRO acts by antagonizing serotonin, these data may give support to the idea of serotoninergic control of cortisol secretion.

The effect of hypoglycemia on hypothalamic thyrotropin-releasing hormone (HRH) in the rat.

A rapid radioimmunoassay for TRH with a high degree of specificity and sensitivity is described. The procedure is capable of measuring TRH in amounts less than 15 pg/tube. Such an assay system has enabled us to study the effect of hypoglycemia on hypothalamic TRH content. Forty-eight female, adult Holtzman rats were divided into 8 groups of 6. Regular insulin was injected intraperitoneally into each rat except for the basal group. A separate batch of similar rats was studied in the same fashion except that saline was injected instead of insulin. Each group of rats was decapitated and the trunk blood collected at 0, 15, 30, 45, 60, 90, 120 and 180 min post-injection. Appropriate tissues were rapidly taken and immediately extracted in ice-cold methanol. Hypothalamic TRH, pituitary TSH, serum TSH and serum triiodothyronine (T3) and thyroxine (T4) were serially determined. In the insulin-treated group, a rapid fall in blood sugar was observed reaching a nadir in 15 min. Hypothalamic TRH fell from a basal mean +/- SE value of 3.25 +/- 0.31 ng to 1.54 +/- 0.14 ng/hypothalamus (P less than 0.01). Pituitary TSH decreased from 10.0 +/- 0.9 mug to a low of 2.6 +/- 0,8 mug/pituitary (P less than 0.02) at 30 min postinsulin. Serum TSH increased from a basal level of 42.5 +/- 20.5 muU/mo to a peak of 102.1 +/- 10.0 muU/ml 45 min (P less than 0.05) after insulin administration. The incremental change in serum T3 occurred at 90 min when T3 levels increased from a baseline of 107.5 +/- 53.7 ng/100 ml to a peak of 711.7 +/- 20.2 ng/100 ml (P less than 0.01). No changes in T4 were observed. The control group of rats did not show significant changes in hypothalamic TRH. The results of the study indicate that hypoglycemia can induce depletion (presumably release) of hypothalamic TRH with a consequent cascade stimulation of the pituitary-thyroid axis.

Insulin control of hepatic glucose production.

Insluin injected intravenously caused a rapid, marked decrease in hepatic glucose secretion in the rabbit, as determined by an isotope-dilution procedure. This was associated with a decrease in the concentrations of gluconeogenic intermediates from phosphoenolpyruvate to triose phosphates, inclusive, compatible with inhibition of gluconeogenesis at phosphoenolpyruvate carboxykinase. The concentration of glucose 6-phosphate was unaltered but that of hepatic glucose was reduced. The specific activities of the hexose phosphates, relative to that of liver glucose, were the same in control and insulin-treated animals. These observations can be explained by a decrease in the activity of glucose-6-phosphatase. It is concluded that this enzyme is a control point for hepatic glucose production and is inhibited by insulin. In the rat, insulin produced a rapid fall in blood sugar. The hepatic glucose output remained normal despite a fall in hepatic glucose 6-phosphate concentration during the initial period of insulin action. This suggests that glucose-6-phosphate returned to normal with no change in the rate of glucose production. The data suggest that in the rat, insulin produces a transient increase in glucose-6-phosphatase activity.

Subcutaneous glucagon as a test of the ability of the pituitary to secrete GH and ACTH.

SUMMARYThe response to the subcutaneous injection of glucagon (1 mg) has been studied as a test of the ability of the pituitary to secrete ACTH and growth hormone (GH). Tests have been performed on fifteen normal subjects or patients with unrelated conditions, nine patients with pituitary tumours and seventeen with acromegaly. It is suggested that a normal response is a peak level of 5 ng/ml or more of GH (standard NIH GH 1216C) and either a rise of plasma cortisol measured by competitive protein binding of at least 4 μg/100 ml or a peak level of 7 μg/100 ml. In seventeen patients the responses were compared with those obtained in the insulin hypoglycaemia test and there was good agreement. Measurement of plasma ACTH showed that the response is at pituitary and not adrenal cortical level. Peak responses of ACTH and GH were obtrained at 150 min and of cortisol at 180 min. Plasma glucagon concentrations were falling steadily by this time although still above the control level. The mechanism of action of glucagon is not clear but does not appear to be related to fall of blood sugar. The subcutaneous injection of glucagon is not without side effects; about half the patients were nauseated and nine vomited. Nevertheless we believe that a subcutaneous glucagon test is of value for testing the pituitary reserve of ACTH and GH in situations where insulin hypoglycaemia cannot be used.

Transient accommodative paralysis and hyperopia in diabetes.

Transient paralysis of accommodation developed in a 7-year-old diabetic four days after beginning treatment with insulin. Symptomatology this severe is rare in diabetes, and only five similar cases have been reported. However, this case serves as a reminder that milder changes in both refraction and accommodation are frequent at the onset of diabetes (most often after treatment has been started) and may be associated with either a rise or fall in blood sugar.

The effect of diazepam on pituitary function in man.

SUMMARY The integrity of pituitary—adrenal function and growth hormone production was determined in 15 patients before and after treatment with diazepam (30 mg daily). There was no evidence of impairment; nor was the urinary excretion of catecholamines significantly altered. The reproducibility of the plasma corticosteroid response to insulin-induced hypoglycaemia was separately assessed and both the degree of fall in blood sugar and the rise in plasma corticosteroid level were found to be similar.

CHANGES IN INSULIN SECRETION DURING OPEN HEART SURGERY

Metabolic changes are described in 8 patients undergoing cardiopulmonary bypass. During operation there was a failure of insulin response to the glucose used in the bypass pump priming. After the bypass procedure there was a peak in insulin levels associated with a fall in blood sugar and serum potassium levels. Other possible causes of a fall in serum K+ levels such as alkalosis and urinary loss of K+ were excluded. It is suggested that the delayed insulin response to glucose may be due to an increase in catecholamine secretion induced by the trauma of surgery and hypothermia. The clinical significance of these changes is discussed.

CARBOHYDRATE METABOLISM IN PREGNANCY

ABSTRACT The effects of pregnancy and dietary status upon the blood sugar response to exogenous insulin in the rat were evaluated. Unanaesthetized 19-day pregnant, postpartum, and age-matched virgin rats were challenged with intravenous insulin (10 U/kg) after unrestricted access to food or fasting for 48 hours. Appropriate control studies were instituted to correct for the effects of 'handling' upon blood sugar. Fed as well as fasted pregnant rats displayed diminished absolute hypoglycaemic responses to insulin and attenuated rates of blood sugar fall. The relative resistance of pregnant rats to the blood sugar lowering actions of insulin was documented during group comparisons with virgin rats as well as upon reexamination of the same animals postpartum.

The Effect of Dialysis on the Carbohydrate Intolerance of Chronic Renal Failure

Oral glucose tolerance tests were performed in relation to hemodialysis and peritoneal dialysis. The results have shown lower fasting blood sugars and considerably improved glucose tolerance in the immediate post-dialysis period. Both basal serum insulin levels and the rise following glucose were enhanced after hemodialysis. On the other hand, peritoneal dialysis resulted in lower insulin levels. Although there were no consistent changes in the elevated growth hormone concentrations after either dialysis, higher levels were more frequently observed in patients undergoing peritoneal dialysis. In all subjects, plasma-free fatty acids supressed promptly after glucose administration. Following hemodialysis, there was a greater fall in blood sugar in response to tolbutamide, but his was not associated with an enhanced insulin response. Progressive improvement in glucose tolerance occurred in one subject tested serially after renal transplantation. The causes and significance of these metabolic abnormalities in uremic patients are discussed.