Effects of Telfairia Occidentalis Leaf Extract on Plasma Lactate and Liver Glycogen in Rats.

Telfairia occidentalis is a green vegetable popularly consumed among the native of Africa and it is generallybelieved to be of medicinal and nutritional value. Studies have reported its hypoglycaemic and hyperglycaemic effects inrats. In addition to these conflicting reports, the mechanisms for its effects on blood glucose remain inconclusive. Theobjective of this study was to investigate the mechanism involved in the increased blood glucose following treatment withT. occidentalis. Twenty five (25) male albino rats (200-250g) were randomly divided into 5 groups (n=5/group). Rats in thecontrol group received normal saline while rats in other groups were orally treated with 100 or 200 mg/kg body weight ofthe extract for either 1 or 2 weeks. At the end of the treatment, the rats were anaesthetized and blood samples were collectedfor the estimation of some biochemical parameters. The results showed significant decreases in plasma glucose after 1 weekof treatment with 100 mg/kg and 200 mg/kg. However, after 2 weeks of treatment with both doses, plasma glucose levelsincreased significantly and were higher than those of the control and the rats treated for 1 week with both doses. There werealso dose- and duration-dependent decreases in glycogen concentration in the treated rats, especially those treated for twoweeks. Glucose-6-phosphatase activity and liver glycogen concentration were lower in rats treated for 2 weeks whencompared with those treated for 1 week with both doses. Moreover, plasma lactate concentration was lower in the treatedgroups when compared with control. The results suggest that Telfairia occidentalis-induced lowering of plasma glucose afterone week of treatment probably favoured lactate oxidation/gluconeogenesis and elicited breakdown of liver glycogen whichresulted in increased plasma glucose after two weeks of treatment.

Intestinal glucose uptake responses to infusion of glucose, fructose and galactose in dogs Intestinal glucose uptake responses to infusion of glucose, fructose and galactose in dogs.

The present study was designed to investigate the effects of intravanous (i.v) infusion of fructose, galactose and glucose on canine IGU during postprandial state. Experiments were carried out on fasted, male, anaesthethized adult mongrel dogs divided into four groups with 5 dogs per group. Each of the groups was given i.v infusion of normal saline, fructose (0.15, 0.55 and 1.1mg/dl/min), galactose (0.15, 0.55 and 1.1mg/dl/min) and glucose (0.15, 0.55 and 1.1mg/dl/min) respectively. Through a midline laparatomy, the upper jejunum was secured and cannulated for blood flow measurement. Blood samples were obtained for measurement of glucose content of arterial and venous blood from the upper jejunal segment. The blood glucose was determined by glucose oxidase method and intestinal glucose uptake was calculated as the product of jejunal blood flow and arterio-venous glucose difference. Values are means ± S.E.M, compared by ANOVA and Student t-test. Fructose, galactose and glucose significantly increased arterial blood glucose from 97.60 ± 1.78 mg/dl to 114.20 ± 1.88, 109.80 ± 1.43, and 141.20 ± 5.65 mg/dl, respectively. Glucose also significantly increased jejunal blood flow from 10.0 ± 0.32 ml/min to 14.40 ± 0.93 ml/min, however, fructose and galactose did not produce any significant effect on intestinal blood flow. IGU increased by 600%, 350%, and 700% in response to fructose, galactose and glucose respectively. There is no correlation between the increase in blood glucose levels induced by each of the sugars and its corresponding rise in IGU. The data suggest that the intestine responds to fructose and galactose in a similar manner as glucose probably through similar mechanism.

Role of Adrenergic Receptors in Glucose, Fructose and Galactose-Induced Increases in Intestinal Glucose Uptake in Dogs.

The study investigated the role of adrenergic receptors in glucose, fructose-, and galactose- induced increases in intestinal glucose uptake. Experiments were carried out on fasted male anaesthetized Nigerian local dogs divided into seven groups (with five dogs per group). Group I dogs were administered normal saline and served as control. Dogs in groups II, III and IV were intravenously infused with glucose (1.1 mg/kg/min), fructose (1.1 mg/kg/min) and galactose (1.1 mg/kg/min) respectively. Another three groups, V, VI and VII were pretreated with prazosin (0.2mg/kg), propranolol (0.5mg/kg) or a combination of prazosin (0.2mg/kg) and propranolol (0.5mg/kg) followed by glucose infusion, frutose infusion or galactose infusion respectively. Through a midline laparatomy, the upper jejunum was cannulated for blood flow measurement and blood samples were obtained for measurement of glucose content of the arterial blood and venous blood from the upper jejunal segment. Glucose uptake was calculated as the product of jejunal blood flow and the difference between arterial and venous glucose levels (A-V glucose). The results showed that pretreatment of the animal with prazosin had no effect on glucose and galactose induced increases in glucose uptake. However, pretreatment with propranolol completely abolished glucose, fructose and galactose-induced increases in intestinal glucose uptake. Prazosin also significantly reduced galactose-induced increase in intestinal glucose uptake. The results suggest that the increases in intestinal glucose uptake induced by glucose and fructose are mediated mostly by beta adrenergic receptors while that of galactose is mediated by both alpha and beta adrenergic receptors.

Adiponectin and E-selectin concentrations in relation to inflammation in obese type 2 diabetic patients with coronary heart disease(s).

AIM: Adipose tissue is now regarded as a source of proinflammatory mediators which may contribute to vascular injury, insulin resistance (IR), and atherogenesis, however, some of them have a protective role against vascular inflammation and/or IR; namely adiponectin and nitric oxide (NO). Adiponectin is a fat derived hormone, which enhances insulin sensitivity. In experimental studies adiponectin was shown to have anti-atherogenic properties by suppressing endothelial expression of adhesion molecules as endothelial-selectin (E-selectin) and inflammatory cytokines as high-sensitivity C-reactive protein (hsCRP), interleukin-1ß (IL-1ß), and monocyte chemotactic protein-1 (MCP-1). Therefore, the aim of the study was to evaluate plasma adiponectin, E-selectin, hsCRP, IL-1ß, and MCP-1 concentrations in obese patients with and without coronary heart disease (CHD) having type 2 diabetes mellitus (DM) and evaluation of their relationship with selected anthropometric, biochemical, and clinical parameters. METHODS: The study group consisted of (N.=70) males, 20 of which served as healthy non-obese controls (group I) (mean age 38.5±3.7 years; mean BMI 28±1.2 kg/m2). Patients enrolled in the study were classified into the following groups: type 2 DM obese subjects without CHD (group II) (N.=25) (mean age 42.2±3 years; mean BMI 32.1±1.4 kg/m2) and type 2 DM obese subjects with CHD (group III) (N.=25) (mean age 40.6±3 years; mean BMI 31.5±1.2 kg/m2). Glucose and insulin estimation was performed and insulin resistance index (HOMA-IR) was calculated. In the fasting state, the plasma HbA1c, adiponectin, E-selectin, in comparison to hsCRP, IL-1ß, MCP-1, and lipid parameters were estimated. RESULTS: FBG, HbA 1c %, lipids, insulin, MDA, NO, hsCRP, IL-?, MCP-1, Adiponectin as well as E-selectin concentration were significantly different in patients with type 2 DM and CHD in comparison to patients without CHD and moreover, the healthy control group (P=0.01). There was a significant negative correlation between adiponectin and E-selectin (r=-0.642; P=0.0001). CONCLUSION: Our study supports the hypothesis that decreased level of adipokine(s), together with increased oxidative stress, pro-inflammatory marker(s) as well as endothelial adhesion molecule(s) contributes to the complex process of atherosclerosis in type 2 diabetic obese patients that may lead eventually to CHD.

Effect of photoperiod on testicular functions in male Sprague-Dawley rats.

Variation in reproductive status in response to photoperiods has been observed in laboratory rats. We investigated the effects of photoperiod on testicular activity in Sprague-Dawley rats (Rattus norvigicus) maintained in experimental photoperiodic condition. Twenty-four adult male rats weighing 170+/-10g were conditioned to different lighting conditions of Light/Dark (LD) Cycle for 6 weeks. Group 1, Control group (LD12:12, light on from 07:00hr to 19:00hr). Group 2, Short Photoperiod group (LD 8:16hr, light on from 09:00hr to 17:00hr). Group 3, Long Photoperiod group (LD 16:8hr, light on from 05:00hr to 21:00hr). A significant influence of different lighting conditions on the testicular parameters was observed. Short photoperiod showed a suppressing effect (P < 0.001) on testicular weight, sperm motility sperm viability and sperm counts, while long photoperiod had an inducing, though insignificant, effect on the measured parameters. The results confirmed that Sprague-Dawley rats are photoresponsive and changes in the photoperiod could influence their reproductive functions.

Propionyl-L-carnitine as protector against adriamycin-induced cardiomyopathy.

Propionyl- l -carnitine (PLC) is a naturally occurring compound that has been considered for the treatment of many forms of cardiomyopathies. In this study, the possible mechanisms whereby PLC could protect against adriamycin (ADR)-induced cardiomyopathy were carried out. Administration of ADR (3 mg kg(-1)i.p., every other day over a period of 2 weeks) resulted in a significant two-fold increase in serum levels of creatine phosphokinase, lactate dehydrogenase and glutamic oxaloacetic transaminase, whereas daily administration of PLC (250 mg kg(-1), i.p. for 2 weeks) induced non-significant change. Daily administration of PLC to ADR-treated rats resulted in complete reversal of ADR-induced increase in cardiac enzymes except lactate dehydrogenase which was only reversed by 66%. In cardiac tissue homogenate, ADR caused a significant 53% increase in malonedialdehyde (MDA) and a significant 50% decrease in reduced glutathione (GSH) levels, whereas PLC induced a significant 33% decrease in MDA and a significant 41% increase in GSH levels. Daily administration of PLC to ADR-treated rats completely reversed the increase in MDA and the decrease in GSH induced by ADR to the normal levels. In rat heart mitochondria isolated 24 h after the last dose, ADR induced a significant 48% and 42% decrease in(14)CO(2)released from the oxidation of [1-(14)C]palmitoyl-CoA and [1-(14)C]palmitoylcarnitine, respectively, whereas PLC resulted in a significant 66% and 54% increase in the oxidation of both substrates, respectively. Interestingly, administration of PLC to ADR-treated rats resulted in complete recovery of the ADR-induced decrease in the oxidation of both substrates. In addition, in rat heart mitochondria, the oxidation of [1-(14)C]pyruvate, [1-(14)C]pyruvate and [1-(14)C]octanoate were not affected by ADR and/or PLC treatment. Moreover, ADR caused severe histopathological lesions manifested as toxic myocarditis which is protected by PLC. Worth mentioning is that PLC had no effect on the antitumour activity of ADR in solid Ehrlich carcinoma. Results from this study suggest that: (1) in the heart, PLC therapy completely protects against ADR-induced inhibition of mitochondrial beta -oxidation of long-chain fatty acids; (2) PLC has and/or induces a powerful antioxidant defense mechanism against ADR-induced lipid peroxidation of cardiac membranes; and finally (3) PLC has no effect on the antitumour activity of ADR.