Hypoglicemic and Hypolipedimic Effects of Ganoderma lucidum in Streptozotocin-Induced Diabetic Rats

Background:Ganoderma lucidum (Leyss. Ex. Fr) Karst is a basidiomycete mushroom that has been used for many years as a food supplement and medicine. In Brazil, National Health Surveillance Agency (ANVISA) classified Ganoderma lucidum as a nutraceutical product. The objective of the present work was to observe the effects of an extract from Ganoderma lucidum in rats treated with streptozotocin, and an agent that induces diabetes. Method: Male Wistar rats were obtained from the animal lodging facilities of both University Nove de Julho (UNINOVE) and Lusiada Universitary Center (UNILUS) with approval from the Ethics Committee for Animal Research. Animals were separated into groups: (1) C: Normoglycemic control water; (2) CE: Normoglycemic control group that received hydroethanolic extract (GWA); (3) DM1 + GWA: Diabetic group that received extract GWA; and (4) DM1: Diabetic group that received water. The treatment was evaluated over a 30-day period. Food and water were weighted, and blood plasma biochemical analysis performed. Results: G. lucidum extract contained beta-glucan, proteins and phenols. Biochemical analysis indicated a decrease of plasma glycemic and lipid levels in DM rats induced with streptozotocin and treated with GWA extract. Histopathological analysis from pancreas of GWA-treated DM animals showed preservation of up to 50% of pancreatic islet total area when compared to the DM control group. In plasma, Kyn was present in diabetic rats, while in treated diabetic rats more Trp was detected. Conclusion: Evaluation from G. lucidum extract in STZ-hyperglycemic rats indicated that the extract possesses hypoglycemic and hypolipidemic activities. Support: Proj. CNPq 474681/201.

Effects of Dietary Supplementation withAgaricus sylvaticusSchaeffer on Glycemia and Cholesterol after Streptozotocin-Induced Diabetes in Rats

This study evaluated the effect of theAgaricus sylvaticus(sun mushroom) on biochemical tests of the plasma and on the morphology of the pancreas in an experimental model of type I diabetes mellitus (DM1) induced by streptozotocin. One gram of dryA. sylvaticuswas homogenized and mixed with the chow. Male Wistar rats were allocated as follows: normoglycemic control that received commercial chow; normoglycemic control group that received chow withA. sylvaticus;diabetic group that received commercial chow; and diabetic group that received chow withA. sylvaticus. Weight, food, and water consumption were measured every two days. Blood glucose levels were measured twice a week. After 30 days, the animals were euthanized and blood was collected for the analysis of cholesterol, HDL, triglycerides, blood sugar, glutamic-pyruvic transaminase (GPT), alkaline phosphatase, iron, transferrin, and urea. The pancreas was processed for microscopic analysis.A. sylvaticusmodulated the levels of cholesterol, HDL, triglycerides, blood sugar, GPT, alkaline phosphatase, iron, transferrin, and urea to levels similar to those found in the controls and led to compensatory hyperplasia of the islets of Langerhans.A. sylvaticusis potentially beneficial in the control of type 1 diabetes, and it may also prevent pancreas damage.

Selective hypoglycemia in the liver induces adrenomedullary counterregulatory response

The present study was designed to investigate adrenal medullary responses to a selective regional hypoglycemia in the liver of dogs with hepatic cross-perfusion. The liver of recipient dogs (Rc) was perfused with vena caval and aortic blood of donor dogs (Dn) through the portal vein and hepatic artery, respectively. Total hepatic venous blood of Rc was returned to Dn through the left jugular vein. Upon the cross-perfusion, glucose (Glc, 5%) was infused at an average rate of 3.5 +/- 0.2 mg.kg-1.min-1 (n = 12) in Rc to compensate the loss of hepatic Glc delivery into the systemic circulation. Insulin (5.0 IU/kg i.v.) was administered to Dn followed by infusion with an average rate of 0.95 +/- 0.17 IU kg-1.min-1 (n = 6), and this served as the hepatic hypoglycemic group. Saline was similarly administered to Dn, which served as the normoglycemic control group. In the hepatic hypoglycemic group, aortic and vena caval Glc levels in Dn, which represent Glc concentrations entering the liver of Rc, decreased from 129.9 +/- 7.1 and 122.5 +/- 7.8 to 44.6 +/- 6.1 and 38.0 +/- 5.9 mg/dl (P < 0.05) 45 min after insulin administration, respectively. During this regional hepatic hypoglycemia in Rc, the systemic glycemia being kept within a normal range, adrenal epinephrine and norepinephrine output increased from 245.5 +/- 55.8 and 39.1 +/- 9.9 to 618.9 +/- 180.4 and 134.3 +/- 52.7 ng/min (P < 0.05), respectively. By contrast, aortic Glc and insulin levels in Dn of the normoglycemic control group remained unchanged, as did adrenal epinephrine and norepinephrine output in Rc. The results indicate that the regional hepatic hypoglycemia can significantly increase adrenal catecholamine secretion even during systemic (central) normoglycemia. The study suggests that the hepatoadrenal Glc counter-regulatory reflex may be functionally implicated in insulin-induced hypoglycemia.

Beta-receptor-mediated increase in cerebral blood flow during hypoglycemia

We tested the hypothesis that beta-adrenergic receptor stimulation is involved with the increase in regional cerebral blood flow (rCBF) during hypoglycemia. Rats were surgically prepared with the use of halothane-nitrous oxide anesthesia. A plaster restraining cast was placed around the hindquarters, and anesthesia was discontinued. Hypoglycemia was produced by an intravenous injection of insulin (15 U/kg); normoglycemic control rats were given saline. Propranolol (1.5 mg/kg) was administered to some control and some hypoglycemic rats to block the beta-adrenergic receptors. Regional CBF was measured using 4-[N-methyl-14C]iodoantipyrine. Plasma glucose in the normoglycemic and hypoglycemic groups was approximately 6 and 1.4 mumol/ml, respectively. Regional CBF increased during hypoglycemia in rats that were not treated with propranolol. The increase varied from approximately 60 to 200% depending on the brain region. During hypoglycemia, propranolol abolished the increase in rCBF in the hypothalamus, cerebellum, and pyramidal tract. In other regions the increase in rCBF was only 33-65% of the increase in hypoglycemic rats that were not treated with propranolol. We conclude that beta-receptor stimulation plays a major role in the increase in rCBF during hypoglycemia.

Regional Cerebral and Neural Lobe Blood Flow during Insulin-Induced Hypoglycemia in Unanesthetized Rats

The effects of hypoglycemia on regional cerebral blood flow (rCBF) were studied in awake restrained rats. The rats were divided into three groups consisting of (1) a normoglycemic control group that received only saline, (2) a hypoglycemic group A, which was given insulin 30 min before flow was measured, and (3) a hypoglycemic group B, which was given insulin 90 and 30 min before flow was measured. Regional CBF was measured using 14C-iodoantipyrine. Mean plasma glucose was 8.76 μmol/ml in the control group, 2.63 μmol/ml in hypoglycemic group A, and 1.51 μmol/ml in hypoglycemic group B. Plasma epinephrine and norepinephrine concentrations increased to approximately 375% and 160%, respectively, of control values in hypoglycemic groups A and B. In the hypoglycemic group A, rCBF significantly increased in three brain regions. In the hypoglycemic group B, rCBF increased significantly in all brain regions measured, with the exception of the neural lobe, in which it decreased. The increase in rCBF ranged from 38% in the hypothalamus to 138% in the thalamus. Neural lobe blood flow significantly decreased by 31%. The neural lobe was the only brain region studied that is not protected by a blood-brain barrier. It may be sensitive to changes in the concentration of vasoactive agents in blood, such as epinephrine and norepinephrine.