Effectiveness of osteopathic manipulative applications on hypothalamic-pituitary-adrenal (HPA) axis in youth with major depressive disorder: a randomized double-blind, placebo-controlled trial.

CONTEXT: Osteopathic treatments regulate the neurovegetative system through joint mobilizations and manipulations, and myofascial and craniosacral techniques. Despite the growing body of research, the precise impact of osteopathic medicine on the autonomic nervous system (ANS) is not yet fully elucidated. As to Kuchera's techniques, the stimulation of the sympathetic trunk and prevertebral ganglia contributed to harmonization of the sympathetic activity. However, potential relationships between the harmonization of the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis largely remain uncertain and warrant further exploration. OBJECTIVES: This study was designed to evaluate the effectiveness of the osteopathic sympathetic harmonization (OSH) on the SNS and the HPA axis in youth with major depressive disorder (MDD). METHODS: The study included 39 youths aged 15-21 years and diagnosed with MDD. The participants were randomly assigned into either the OSH or the placebo group. Stimulation was performed on the sympathetic truncus and prevertebral ganglia in the OSH group. The stimulation of the placebo group was performed with a lighter touch and a shorter duration in similar areas. Each participant completed the Beck Depression Inventory (BDI) and the State and Trait Anxiety Inventory (SAI and TAI) before the application. Blood pressure (BP) and pulse measurements were made, and saliva samples were taken before, immediately after, and 20 min after application. RESULTS: The baseline BDI (p=0.617) and TAI (p=0.322) scores were similar in both groups. Although the SAI scores decreased in both groups postintervention, no statistically significant difference was found between the two groups. Subjects who received OSH had a decrease in α-amylase level (p=0.028) and an increase in cortisol level (p=0.009) 20 min after the procedure. CONCLUSIONS: Following OSH application in depressed youth, SNS activity may decrease, whereas HPA axis activity may increase. Future studies may examine the therapeutic efficacy of repeated OSH applications in depressed individuals.

The effect of temozolomide on the prevention of epidural fibrosis developing after lumbar laminectomy in rats.

AIM: Failed back surgery syndrome is observed in 15% of patients who have undergone surgery for lumbar disk hernia.Excess epidural fibrosis is the etiology in 24% of FBSS cases. This study was conducted with the belief that the antiproliferative effect of temozolomide can prevent epidural fibrosis. MATERIAL AND METHODS: 8 rats (Group I) underwent laminectomy and were then administered saline while 6 rats (Group II) were administered temozolomide at a dose of 18 mg/kg/day for 5 days after the surgery to make up a total of 14 male Wistar rats used. The pathology preparations of subjects sacrificed at the end of week 6 were histopathologically examined with the Hematoxylin-Eosin stain and Trichrome stain. The pathology preparations were assessed with the analysis parameters and scale generated by He et al. The results were analyzed with the Chisquare test. RESULTS: No significant difference was found between the two groups in terms of bone and cartilage regeneration, arachnoidal fibrosis, and inflammatory and fibroblast cell densities. Epidural fibrosis formation was significantly less and there was no grade III fibrosis in the Temozolomide group. This was found to be statistically significant (p=0.0302). No side effect of dural or intradural damage was observed. CONCLUSION: Temozolomide was found to be effective in preventing epidural fibrosis. However, further research is required to determine its effectiveness in local applications and the appropriate dose range.

The effect of radiofrequency radiation on DNA and lipid damage in female and male infant rabbits.

PURPOSE: We aimed to design a prolonged radiofrequency (RF) radiation exposure and investigate in an animal model, possible bio-effects of RF radiation on the ongoing developmental stages of children from conception to childhood. MATERIALS AND METHODS: A total of 72 New Zealand female and male white rabbits aged one month were used. Females were exposed to RF radiation for 15 min/day during 7 days, whereas males were exposed to the same level of radiation for 15 min/day during 14 days. Thirty-six female and 36 male infant rabbits were randomly divided into four groups: Group I [Intrauterine (IU) exposure (-); Extrauterine (EU) exposure (-)]: Sham exposure which means rabbits were exposed to 1800 MHz Global System for Mobile Telecommunication (GSM)-like RF signals neither in the IU nor in the EU periods. Group II [IU exposure (-); EU exposure (+)]: Infant rabbits were exposed to 1800 MHz GSM-like RF signals when they reached one month of age. Group III [IU exposure (+); EU exposure (-)]: Infant rabbits were exposed to 1800 MHz GSM-like RF signals in the IU period (between 15th and 22nd days of the gestational period). Group IV [IU exposure (+); EU exposure (+)]: Infant rabbits were exposed to 1800 MHz GSM-like RF signals both in the IU period (between 15th and 22nd days of the gestational period) and in the EU period when they reached one month of age. Biochemical analysis for lipid peroxidation and DNA damage were carried out in the livers of all rabbits. RESULTS: Lipid peroxidation levels in the liver tissues of female and male infant rabbits increased under RF radiation exposure. Liver 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels of female rabbits exposed to RF radiation were also found to increase when compared with the levels of non-exposed infants. However, there were no changes in liver 8-OHdG levels of male rabbits under RF exposure. CONCLUSION: Consequently, it can be concluded that GSM-like RF radiation may induce biochemical changes by increasing free radical attacks to structural biomolecules in the rabbit as an experimental animal model.

Basal damage and oxidative DNA damage in children with chronic kidney disease measured by use of the comet assay.

One consequence of chronic kidney disease (CKD) is an elevated risk for cancer. There is sufficient evidence to conclude that there is an increased incidence of at least some cancers in kidney-dialysis patients. Cancer risk after kidney transplantation has mainly been attributed to immunosuppressive therapy. There are no data evaluating DNA damage in children with CKD, in dialysis patients, or following kidney transplantation. In this study, the comet assay and the enzyme-modified comet assay - with the use of endonuclease III (Endo III) and formamidopyrimidine glycosylase (FPG) enzymes - were conducted to investigate the basal damage and the oxidative DNA damage as a result of treatment in peripheral blood lymphocytes of children. Children at various stages of treatment for kidney disease, including pre-dialysis patients (PreD) (n=17), regular hemodialysis patients (HD) (n=15), and those that received kidney transplants (Tx) (n=17), comprised the study group. They were compared with age- and gender-matched healthy children (n=20) as a control group. Our results show that the %DNA intensity, a measure of basal damage, was significantly increased in children with CKD (mean ± SD) (5.22 ± 1.57) and also in each of the PreD, HD, and Tx groups [(4.92 ± 1.23), (4.91 ± 1.35), and (5.79 ± 1.94), respectively, vs the healthy children (2.74 ± 2.91) (p<0.001). Significant increases in oxidative DNA damage were only found in the FPG-sensitive sites for the PreD and Tx groups, compared with control and HD groups (p<0.05), suggesting that basal DNA damage was more evident for the PreD, HD, and Tx groups. The findings of the present study indicate a critical need for further research on genomic damage with different endpoints and also for preventive measures and improvements in treatment of pediatric patients, in order to improve their life expectancy.

Micronucleus frequencies in peripheral blood lymphocytes of children with chronic kidney disease.

One of the crucial adverse effects of chronic kidney disease (CKD) and its treatment is an elevated cancer risk. There are no data on cytogenetic effects in children with CKD or children undergoing dialysis or those who have received a transplant. In this study, cytogenetic effects in children with CKD in pre-dialysis (PreD) stage, on regular haemodialysis (HD) and transplanted (Tx) compared with a control group of healthy children has been investigated using the cytokinesis-blocked micronucleus (CBMN) assay and fluorescence in situ hybridisation (FISH) combined with CBMN (CBMN-FISH) in peripheral blood lymphocytes. The results revealed a significant increase (P < 0.001) in micronucleus (MN) frequencies [mean ± SD (n)] in the PreD, HD and Tx groups versus the control group [CBMN assay; 9.19 ± 2.61 (16), 9.07 ± 4.86 (15), 6.12 ± 5.33 (17) versus 1.60 ± 0.99 (20), respectively]. Moreover, centromere negative micronucleus (C- MN) and centromere positive micronucleus (C+ MN) frequencies were significantly higher in each subgroup children (PreD, HD and Tx) than in the control group (P < 0.01) although children in Tx group had lower C- MN frequencies than PreD and lower C+ MN frequencies than PreD and HD groups (P < 0.05). Additionally, MN frequencies in mononuclear cells, nucleoplasmic bridges and nuclear buds in binucleated cells were increased in children with CKD (P < 0.001, P < 0.001, P > 0.05, respectively). The nuclear division index significantly decreased in Tx group relative to the control, PreD and HD groups (P < 0.001). Associations between cytogenetic parameters and creatinine or blood urea nitrogen were found (P < 0.05). To provide longer and better life expectancy of children with CKD and treatment modes, further research is needed to better understand and avoid these effects.

Resveratrol shows vasoprotective effect reducing oxidative stress without affecting metabolic disturbances in insulin-dependent diabetes of rabbits.

PURPOSE: Resveratrol has been shown to have vasoprotective effects by upregulating oxidative defense mechanisms in a variety of pathophysiological conditions. However, the effect of resveratrol on diabetic oxidative stress and vascular and metabolic abnormalities is not completely understood. Therefore, this study was designed to evaluate whether long-term resveratrol supplementation has a protective effect on vascular function and integrity in association with metabolic parameters and oxidative stress in insulin-dependent diabetes. METHODS: Diabetes was induced in rabbits with alloxan and maintained for 8 weeks. We used a resveratrol dose of 5 mg/L (10 weeks, starting 14 days before alloxan injection) and 50 mg/L (8 or 10 weeks, starting concomitantly or 14 days before alloxan injection) in the drinking water of rabbits. RESULTS: Relaxation to acetylcholine was impaired (control 75.6 ± 3.59%, versus diabetic 42.23 ± 2.53%) and contractions to phenylephrine increased (control 136.89 ± 2.27%, versus diabetic 159.37 ± 6.27%) in aortas from diabetic animals. These changes were associated with increased basal or NAD(P)H-induced superoxide production, as well as lipid peroxide and superoxide dismutase (SOD) levels in the aortic samples. The maximal relaxation to acetylcholine improved by 75.74 ± 9.04% in diabetic rabbits treated with resveratrol. The increased contractions to phenylephrine were not restored to control values after resveratrol treatments, but sensitivity to the contractions tended to decrease. Resveratrol increased nitrite/nitrate levels and suppressed basal or NAD(P)H-induced superoxide production and lipid peroxide levels in the aortas. Importantly, resveratrol increased serum insulin levels without affecting blood glucose and the lipid profile in diabetic rabbits. Using electron microscopic examinations, resveratrol was found to markedly protect the endothelial integrity from diabetes. CONCLUSION: Overall, there was no noticeable difference between resveratrol treatment groups on the recovery from diabetes. Our results indicate that resveratrol alleviates type 1 diabetes-induced vasculopathy by decreasing vascular oxidative stress and thereby increasing the bioavailability of nitric oxide without changing metabolic abnormalities.

Infliximab administration reduces neuronal apoptosis on the optic pathways in a rabbit hydrocephalus model: a preliminary report.

OBJECT: This study was designed to explore the effects of infliximab on the optic pathway in kaolin induced hydrocephalus rabbit model. METHODS: After injection of kaolin to the cisterna magna of 12 New Zealand rabbits for induction of hydrocephalus, animals were divided into 2 groups and received either infliximab or normal saline. The intracranial pressure measurement was performed 2 times; firstly, before kaolin injection and secondly, before decapitation to ensure that the rabbits had hydrocephalus. After 2 weeks, animals were decapitated. RESULTS: Apoptotic cells in the lateral geniculate body, optic radiation, and optic disc were counted with TUNEL method. Apoptotic cell counts of the lateral geniculate body and the optic radiation were showed statistically significant difference between the infliximab group and the control group. CONCLUSIONS: This study suggests that infliximab may have a neuroprotective effect through its anti-apoptotic property on hydrocephalus induced optic pathways injury.

Resveratrol supplementation gender independently improves endothelial reactivity and suppresses superoxide production in healthy rats.

PURPOSE: Resveratrol, a polyphenolic compound mainly abundant in red wines, has beneficial cardiovascular effects on various pathological conditions. However, at present, the effect of resveratrol on health promotion remains unclear. Therefore, in this study, we assessed whether long-term resveratrol supplementation changes endothelial function, vascular contractility, nitric oxide and superoxide production in healthy male and female rats. METHODS: Wistar rats were treated with resveratrol (50 mg/l) in their drinking water for 3 weeks. We investigated relaxation to acetylcholine (10(-9)-10(-4) M) and contractions to phenylephrine (10(-9)-3 x 10(-4) M) and angiotensin II (10(-10)-10(-5) M) in either endothelium-intact or denuded aortae from control and resveratrol-treated male and female rats. Aortic superoxide production capacity was measured in response to provocation by angiotensin II and NAD(P)H. Plasma nitrite/nitrate levels and superoxide dismutase (SOD) activity were also evaluated. RESULTS: Resveratrol supplementation gender independently increased relaxation to acetylcholine and decreased contractions to phenylephrine and angiotensin II in endothelium-intact aortic rings, but not in endothelium-denuded arteries, from healthy male and female rats. This was associated with increased plasma nitrite/nitrate levels. Furthermore, resveratrol caused a refractoriness to angiotensin II and NAD(P)H-induced provocation in superoxide production. CONCLUSION: Our results suggest that resveratrol supplementation gender independently could improve the capacity of endothelial function and suppression of oxidative stress under physiological conditions. Resveratrol ingestion indicates a potential for cardiovascular health promotion.

Oxidant/antioxidant balance in patients with thyroid cancer

PURPOSE: To compare the antioxidant enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of lipid peroxidation product malondialdehyde (MDA) in blood samples of thyroid cancer patients compared to healthy controls. METHODS: 43 control subjects (mean age 44±13 years) and 43 patients (43±13 years) presented with multinodular goiter whose fine needle aspiration revealed malignant cytology were included into this study. The SOD, MDA and GSH-Px activities were measured in control subjects, and before/20 days after thyroidectomy in thyroid cancer patients. RESULTS: SOD activities of pre-thyroidectomy, post-thyroidectomy and control groups were not different (p>0.05). Before thyroidectomy GSH-Px activities were lower (p<0.05) and MDA levels were higher (p<0.05) than the control group. In post- thyroidectomy, GSH-Px activity (p<0.05) increased, and MDA levels (p<0.05) decreased compared to prethyroidectomy levels. After thyroidectomy GSH-Px activity was significantly higher than the control group (p<0.05). Although post-thyroidectomy MDA levels significantly decreased, they were still higher than the control group (p<0.05). CONCLUSION: The superoxide dismutase does not seem to change with thyroid cancer and thyroidectomy but both antioxidant glutathione peroxidase and lipid peroxidation product malondialdehyde do. These preliminary findings may point out oxidant/antioxidant imbalance associated with thyroid cancer.

Oxidant/antioxidant balance in patients with thyroid cancer.

PURPOSE: To compare the antioxidant enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the levels of lipid peroxidation product malondialdehyde (MDA) in blood samples of thyroid cancer patients compared to healthy controls. METHODS: 43 control subjects (mean age 44+/-13 years) and 43 patients (43+/-13 years) presented with multinodular goiter whose fine needle aspiration revealed malignant cytology were included into this study. The SOD, MDA and GSH-Px activities were measured in control subjects, and before/20 days after thyroidectomy in thyroid cancer patients. RESULTS: SOD activities of pre-thyroidectomy, post-thyroidectomy and control groups were not different (p>0.05). Before thyroidectomy GSH-Px activities were lower (p<0.05) and MDA levels were higher (p<0.05) than the control group. In post- thyroidectomy, GSH-Px activity (p<0.05) increased, and MDA levels (p<0.05) decreased compared to prethyroidectomy levels. After thyroidectomy GSH-Px activity was significantly higher than the control group (p<0.05). Although post-thyroidectomy MDA levels significantly decreased, they were still higher than the control group (p<0.05). CONCLUSION: The superoxide dismutase does not seem to change with thyroid cancer and thyroidectomy but both antioxidant glutathione peroxidase and lipid peroxidation product malondialdehyde do. These preliminary findings may point out oxidant/antioxidant imbalance associated with thyroid cancer.

Advanced oxidation protein products, ferrous oxidation in xylenol orange, and malondialdehyde levels in thyroid cancer.

AIMS AND BACKGROUND: The oxidation of protein plays an essential role in the pathogenesis of an important number of degenerative and cancer diseases, which is now widely recognized. The aim is to examine advanced oxidation protein products (AOPPs), lipid peroxidation products malondialdehyde (MDA), and ferrous oxidation in xylenol orange (FOX) in blood samples of papillary thyroid cancer patients compared with healthy controls to determine the oxidation status and the change after thyroidectomy. METHODS: Thirty-five female thyroid cancer patients who underwent total thyroidectomy and 39 female control subjects were included into this study. Prethyroidectomy and postthyroidectomy, AOPP, FOX, and MDA levels were studied. RESULTS: Prethyroidectomy AOPP, FOX, and MDA levels were significantly higher compared to control (P < .05). In postthyroidectomy AOPP, FOX, and MDA levels were significantly decreased compared with prethyroidectomy levels (P < .05). However, postthyroidectomy levels on the 20th day were still significantly higher, compared to control subjects (P < .05). CONCLUSION: In conclusion, all of AOPP, FOX, and MDA levels that are markers of protein oxidation and lipid hyperoxidation may induce thyroid cancer development and begin to decrease after thyroidectomy.

Assessment of homocysteine, neopterin and nitric oxide levels in Behçet's disease.

BACKGROUND: Behçet's disease is a multisystemic immunoinflammatory disease with a wide variety of clinical manifestations, whereas recurrent aphthous stomatitis is a local oral disease. The aim of this study was to examine the distribution of homocysteine levels in patients with active Behçet's disease, possible association of homocysteine with nitric oxide and neopterin levels, and to characterize the differences between patients with Behçet's disease and those with recurrent aphthous stomatitis in terms of these parameters compared with healthy controls. METHODS: A total of 23 patients with active Behçet's disease, 25 patients with recurrent aphthous stomatitis as positive controls, and 21 healthy subjects were included in this study. Serum homocysteine and neopterin levels were measured flourimetrically by HPLC. Serum nitric oxide production was assayed by measuring total nitrite levels with Griess reagent. RESULTS: Significantly higher homocysteine (12.9+/-3.3 micromol/L) and lower nitric oxide (41.5+/-10.9 micromol/L) and neopterin (6.4+/-1.0 nmol/L) levels were observed in patients with Behçet's disease compared with healthy controls (10.7+/-2.0 micromol/L, 49.7+/-16.2 micromol/L, 8.7+/-2.2 nmol/L, respectively) (p<0.03 for neopterin, p<0.04 for homocysteine and nitric oxide). However, homocysteine, nitric oxide, biopterin and neopterin levels and the neopterin/biopterin ratio for recurrent aphthous stomatitis patients were not significantly different compared to healthy controls. A significant positive correlation was observed between serum homocysteine and serum neopterin/biopterin ratio in patients with Behçet's disease (r=0.975, p<0.005). CONCLUSIONS: In contrast to recurrent aphthous stomatitis, there is a higher prevalence of hyperhomocysteinemia in Behcet's disease. Homocysteine may have deleterious effects on the pathology of Behcet's disease by decreasing nitric oxide levels and interfering with the immune system.

Oxidative status in rheumatoid arthritis.

The insufficiency of antioxidant defense systems and the acceleration of the oxidative reactions can be results of the pro-oxidant/antioxidant imbalance in rheumatoid arthritis (RA). The aim of our study was to investigate the changes in oxidant status by measuring two different parameters; one was the level of malondialdehyde (MDA) as an index of lipid peroxidation and the other was total oxidative status; we could then compare our results with the antioxidant status, superoxide dismutase (SOD) enyzme activities. All were assessed in 22 patients with active RA and 18 age- and gender-matched control subjects. While serum MDA levels were significantly increased in patients with RA compared to the control group (p<0.03), the total oxidative status levels were decreased in patients with RA compared to the control group (p<0.008), and serum SOD activities did not show any statistical difference between the two groups. In conclusion, the increased MDA levels in our study may be important as a marker but are not sufficient to conclude that there was an increase in oxidative stress in RA patients because supporting results were not obtained from SOD and oxidative status measurements. These results give further support to the concept of oxygen free radicals playing a role in the pathogenesis of chronic inflammatory disorders, but we also consider that there is a more complex relationship than has been assumed. We think that further studies are needed to clarify these conflicting results.

Urate oxidation during percutaneous transluminal coronary angioplasty and thrombolysis in patients with coronary artery disease.

Thrombolysis and percutaneous transluminal coronary angioplasty (PTCA) are kinds of procedures that can be used to restore the blood flow of previously ischemic myocardium that can be the result of excessive production of reactive oxygen and nitrogen species, such as superoxide and hydroxyl radical, hypochlorous acid and peroxynitrite. Reaction of urate with some of these potent oxidants results in allantoin production. In this study, we measured the serum allantoin levels, an oxidation product of urate, and "in vivo" marker of free radical generation in reperfusion of ischemic myocardium. After an overnight fasting state, blood samples were collected from 35 patients with coronary occlusive diseases (7 women and 28 men) and 31 healthy subjects (8 women and 23 men). Serum allantoin and urate levels were measured by a GC-MS method. Serum allantoin levels of patients on PTCA therapy (mean+/-SD, 27.4 +/- 15.2 micromol/l) and thrombolytic therapy (24.6 +/- 8.6 micromol/l) were significantly higher than those of the patients without therapy (15.8 +/- 6.2 micromol/l, p < 0.05 with PTCA and p < 0.006 with thrombolysis) and healthy controls (12.6 +/- 6.3 micromol/l, p < 0.002 with PTCA and p < 0.0001 with thrombolysis). Although serum urate levels in PTCA (380.1 +/- 72.6 micromol/l) and thrombolysis (359.5 +/- 60.0 micromol/l) were higher than those in the non-therapy patients (336.6 +/- 53.8 micromol/l) and controls (318.3 +/- 81.0 micromol/l), there were no significant differences among groups (p > 0.05). The results of the study are consistent with others which have demonstrated, higher urate levels are associated with coronary occlusive diseases. Our data support the hypothesis that generation of ROS occurs during myocardial reperfusion. Increased allantoin levels may be used as an index of increased oxidative stress during reperfusion.

Oxidation of uric acid in rheumatoid arthritis: is allantoin a marker of oxidative stress?

Free radicals are implicated in many diseases including atherosclerosis, cancer and also in rheumatoid arthritis. Reaction of uric acid with free radicals, such as hydroxyl radical and hypochlorous acid (HOCl) results in allantoin production. In this study, we measured the serum allantoin levels, oxidation products of uric acid, as a marker of free radical generation in rheumatoid arthritis. Fasting blood samples were obtained from 21 rheumatoid patients and 15 healthy controls. In this study, the serum allantoin and uric acid levels were measured by a gas chromatography-mass spectrometry method and the ratios were calculated. The mean allantoin and uric acid levels and ratios in the patient group were 22.1 +/- 11.3, 280.5 +/- 65.0 and 8.0 +/- 3.7 microM, while in the control group they were 13.6 +/- 6.3, 278.3 +/- 53.6 and 4.9 +/- 2.1 microM, respectively. The effects of gender, age, menopausal status, duration of disease and medications on serum allantoin and uric acid levels of the patient and control groups were studied. Our results suggest that uric acid acts as a free radical scavenger and thus is converted to allantoin. Increased allantoin levels suggest the possible involvement of free radicals in rheumatoid arthritis.

Hypoglycaemic effects of myrtle oil in normal and alloxan-diabetic rabbits.

Myrtus communis L. (Myrtaceae) leaves as well as the volatile oil (Myrtii Oleum; MO) obtained from the leaves are used to lower the blood glucose level in type-2 diabetic patients in Turkish folk medicine. However, little attention has been paid to the therapeutic use of this plant. The present study was designed to investigate the oral hypoglycaemic activity of single and multiple doses of MO in normal and alloxan-diabetic rabbits. MO did not show any effect in normoglycaemic rabbits either in single or multiple dose administrations, but a good hypoglycaemic activity was observed 4 h after the administration to diabetic animals at 50 mg/kg. To investigate the effect of MO on repeated administration in both normal and diabetic rabbits, it was administered in 50 and 100 mg/kg doses once a day for one week. MO significantly lowered blood glucose by 51% in alloxan-diabetic rabbits on the fourth hour and the following days at a dose of 50 mg/kg (P < 0.001). The hypoglycaemic dose (50 mg/kg) was also determined by performing the oral glucose tolerance test (OGTT) in normal rabbits. The hypoglycaemic effect of the MO was 21% higher in rabbits, which received the glucose load orally, when compared with control group. However, MO did not affect serum insulin concentrations in normal and alloxan-diabetic rabbits but reduced the serum triglyceride concentrations by 14% in alloxan-diabetic rabbits. The above observations show that MO exerts hypoglycaemic as well as mild hypotriglyceridemic activity in diabetic animals. The reduction in blood glucose level may be due to the reversible inhibition of alpha-glucosidases present in the brush-border of the small intestinal mucosa, higher rate of glycolysis as envisaged by the higher activity of glucokinase, as one of the key enzymes of glycolysis, and enhanced rate of glycogenesis as evidenced by the higher amount of liver glycogen present after MO administration.