Overweight and obesity in Eastern Morocco: Prevalence and associated risk factors among high school students.

BACKGROUND: Overweight and obesity in children and adolescents have become a major public health problem affecting most countries worldwide. The purpose of the study was to assess the prevalence and risk factors of overweight and obesity among public high school students in Eastern Morocco. METHODS: A cross-sectional survey was conducted between February and May 2014 among a sample of 2271 students (1086 girls and 1185 boys). References from the International Obesity Task Force (IOTF) were used to determine the prevalence of overweight and obesity. RESULTS: The prevalence of overweight and obesity reached 12.2% (14.2% in girls vs 10.4% in boys, P<0.01) and 3.0% (3.1% in girls vs 2.8% in boys), respectively. Risk factors associated with overweight and obesity were urban residence (OR=1.76; [1.18-2.63]; P<0.01), father's income≥5000MAD (OR=1.32; [1.02-1.70]; P<0.05), father's overweight (including obesity) (OR=1.87; [1.38-2.54]; P<0.001) and female sex (OR=1.31; [1.02-1.68]; P<0.05). CONCLUSION: The prevalence of overweight/obesity has reached an alarming rate among high school students in the Eastern region of Morocco. The findings of the present study suggest an urgent need to set up a strategy to prevent and combat this epidemic.

Anti-hypertensive effects of the methanol/methylene chloride stem bark extract of Mammea africana in l-NAME-induced hypertensive rats.

AIM OF THE STUDY: The methanol/methylene chloride (CH(3)OH/CH(2)Cl(2)) extract from the stem bark of Mammea africana was showed to possess vasodilating effect in the presence and the absence of N(omega)-nitro-l-arginine methyl ester (l-NAME). The present study was designed to evaluate the effects of the methanol/methylene chloride from the stem bark of Mammea africana. MATERIALS AND METHODS: The extract (200 mg/(kg day)) was administered orally in rats treated concurrently with l-NAME (40 mg/(kg day)). l-Arginine (100 mg/(kg day)) and captopril (20 mg/(kg day))were used as positive controls. Bodyweight, systolic arterial blood pressure and heart rate were measured weekly throughout the experiment period (28 days). At the end of treatment, animals were killed and the cardiac mass index evaluated. The aorta was used to evaluate the endothelium-dependant relaxation to carbachol. The aorta contraction induced by noradrenalin was also examined and expressed as a percentage of that induced by KCl. RESULTS: The extract neither affected the body weight nor the heart rate. The extract as captopril completely prevented the development of arterial hypertension. Both the substances failed to restore the endothelium-dependent vascular relaxation and increased the vascular contraction to norepinephrine in relation to KCl contraction. They also significantly reduced the left ventricular hypertrophy induced by l-NAME. CONCLUSION: These findings are in agreement with the traditional use of Mammea africana in the treatment of arterial hypertension and indicate that it may have a beneficial effect in patients with NO deficiency but will be unable to improve their endothelium-dependent vasorelaxation.

Effects of Juglans regia Root Bark Extract on Platelet Aggregation, Bleeding Time, and Plasmatic Coagulation: In Vitro and Ex Vivo Experiments.

Platelets have an important role in thrombosis and haemostasis. Hyperactivity of the platelets has been associated with thromboembolic diseases and represents the main cause of complications of cardiovascular diseases. Crude aqueous extract (CAE) of Juglans regia root bark was evaluated for bleeding time, antiaggregant activity by using agonists, thrombin, ADP, collagen, or arachidonic acid (in vitro and ex vivo), and anticoagulant activity by measuring the clotting parameters: activated partial thromboplastin time, prothrombin time, thrombin time, and fibrinogen dosage (in vitro and ex vivo). The result of this study reported that the strongest antiaggregant effect of CAE in vitro was observed on the ADP-induced aggregation with inhibitions up to 90 %, while, in ex vivo experiments, the inhibition (more than 80 %) was observed with all agonists. Anticoagulant effect of CAE significantly prolonged the TT and decreased the fibrinogen level in vitro and ex vivo without interfering with APTT and PT. The bleeding time in mice and rats was significantly increased by CAE. The antiplatelet and anticoagulant effect observed in this study suggest that Juglans regia could have antithrombotic and/or thrombolytic activities and provide an alternative therapy against thrombotic complications related to cardiovascular diseases.

Antihyperglycemic activity of Arbutus unedo, Ammoides pusilla and Thymelaea hirsuta.

The effect of the water extract (WE) of three medicinal plants used as antidiabetic medication in Eastern Morocco (Arbutus unedo: Au, Ammoides pusilla: Ap and Thymelaea hirsuta: Th) was tested in rats with the Oral Glucose Tolerance Test (OGTT) and Intravenous Glucose Tolerance Test (IVGTT). In the OGTT the rats received water, glibenclamide (2 mg/kg) or WE (500 mg/kg for Au and 250 mg/kg for Th and Ap) 30 min before glucose loading (glucose: 1 g/kg). The WE of Au, Ap and Th produced a significant decrease in glycemia after glucose loading. In the IVGTT the WE of Ap and Th produced a significant decrease in glycemia 60 min after i.v. glucose loading (0.5 g/kg). The addition of the WE of Au (500 mg/kg), Ap or Th (250 mg/kg) induced a significant inhibition of jejunal glucose absorption, (31.6%, 28.5% and 40.5% respectively). This effect could explain in part the significant antihyperglycemic effect observed in the OGTT model but it does not exclude other effects on glucose homeostasis, particularly for Ap and Th. Toxicity tests (high LD50 value) suggest no adverse effect of the use of these plants.

Acute diuretic, natriuretic and hypotensive effects of a continuous perfusion of aqueous extract of Urtica dioica in the rat.

This study was performed on anaesthetized male Wistar rats that received a continuous intravenous perfusion during 1.25 h of an aqueous extract of aerial parts of Urtica dioica L. (Urticaceae) at a low dose of 4 mg/kg/h or at a high dose of 24 mg/kg/h, or furosemide (control diuretic) at a dose of 2 mg/kg/h. As compared with a control period in each rat, the arterial blood pressure was reduced proportionally to the dose of the perfusion of the plant extract (15 and 38%, P<0.001, respectively). These effects were accompanied by a correlative increase of diuresis (11 and 84%, P<0. 001, respectively) and natriuresis (28 and 143%, P<0.001, respectively). In the rats perfused by furosemide, the arterial blood pressure was reduced by 28% (P<0.001). The diuresis and natriuresis were also increased proportionally in this case (85 and 155%, P<0.001, respectively). Nevertheless, the hypotensive action of U. dioica was reversible during the recovery periods in about 1 h with the lower dose of the plant extract and furosemide, while the effect of the higher dose was persistent, indicating a possible toxic effect. In conclusion, the results demonstrate an acute hypotensive action of U. dioica that indicates a direct effect on the cardiovascular system. Moreover, diuretic and natriuretic effects were also observed, suggesting an action on the renal function. Finally, the plant extract seems to have a toxic effect at the higher dose.

Phytotherapy of hypertension and diabetes in oriental Morocco.

In order to select the main medicinal plants used in folk medicine to treat arterial hypertension and/or diabetes, a survey was undertaken in different areas of oriental Morocco. The patients (370 women and 256 men) were divided into three groups: diabetics (61%), hypertensives (23%) and hypertensive diabetic persons (16%). On average, 67.51% of patients regularly use medicinal plants. This proportion is perceptibly the same in all groups and does not depend on sex, age and socio-cultural level. This result shows that phytotherapy is widely adopted in northeastern Morocco. For diabetes, 41 plants were cited, of which the most used were Trigonella foenum-graecum L. (Leguminosae), Globularia alypum L. (Globulariaceae), Artemisia herba-alba Asso. (Compositae), Citrullus colocynthis (L.) Schrad. (Cucurbitaceae) and Tetraclinis articulata Benth. (Cupressaceae). In the hypertension's therapy 18 vegetal species were reported, of which the most used were Allium sativum L. (Liliaceae), Olea europea L. (Oleaceae), Arbutus unedo L. (Ericaceae), Urtica dioica L. (Urticaceae) and Petroselinum crispum A.W. Hill (Apiaceae). Among the 18 species used for hypertension, 14 were also employed for diabetes. Moreover, these two diseases were associated in 41% of hypertensives. These findings suggest that hypertension observed in this region would be in a large part related to diabetes.

Hypertensive effects of oral administration of the aqueous extract of Solanum torvum fruits in L-NAME treated rats: evidence from in vivo and in vitro studies.

ETHNOPHARMACOLOGICAL RELEVANCE: Solanum torvum fruits are commonly used in Cameroonian traditional medicine for treatment of arterial hypertension. It has been previously shown that intravenous administration of aqueous extract from dried fruits (AEST) reduced blood pressure. AIM: The present work evaluates acute toxicity and effects of oral administration of AEST in chronic arterial hypertension induced by L-NAME. Effects of AEST were also evaluated on isolated aorta. MATERIALS AND METHODS: AEST (200 mg/kg/day, p.o.) was given solely or concomitantly with L-NAME (40 mg/kg/day, p.o.) for 30 consecutive days. Animal body weight, systolic blood pressure and heart rate were measured before stating the treatment and at the end of each week. Urinary volume and urinary sodium and potassium contents were quantified before and at days 1, 15 and 30 of the treatment. Aorta from treated animals was tested for their sensitivity to noradrenaline and carbachol. Aorta from normal untreated rats was used to evaluate the in vitro vascular effect of AEST. RESULTS: The results showed that AEST did induce neither mortality nor visible signs of toxicity. When given solely or in co-administration with L-NAME, AEST significantly reduced animal's body weight. It amplified the hypertensive and cardiac hypertrophy effect of L-NAME and did not affect these parameters in normotensive animals. AEST increased the sensitivity to noradrenaline in normotensive and significantly reduced it in hypertensive animals. AEST significantly increased urinary volume and sodium excretion in L-NAME treated animals while reducing the sodium excretion in normotensive. In vitro, AEST induced a potent partial endothelium-dependent contraction of aortic ring; contractions that were partially antagonized by prazosin and verapamil and were not relaxed by carbachol. CONCLUSION: These results suggest that oral chronic administration of AEST induced potentiation of arterial hypertension and cardiac hypertrophy in L-NAME treated rats. These effects may result from a reduction in sensitivity to vasorelaxant agents and increase in hypersensitivity to contractile factors. AEST possess potent in vitro vasocontractile activity that may result from activation of both alpha(1)-adrenergic pathway and calcium influx.

The mechanism of positive inotropy induced by adenosine triphosphate in rat heart.

When applied extracellularly in the micromolar range, ATP and related compounds induced a positive inotropy in the rat papillary muscle. This was also true in the rat auricle after pertussis toxin treatment. Then, in both tissues, ATP further increased the contraction after a maximal beta-adrenergic stimulation. The increase in contractile force could be related to the increase in the calcium current. The L-type calcium current was measured by whole-cell patch-clamp recording in single cells isolated from the rat ventricle after the sodium and potassium currents were inhibited by tetrodotoxin and cesium, respectively. When added alone, 10 microM ATP increased the calcium current by 60%. Adenosine 5'-O-(3-thiotriphosphate) was also able to increase calcium current. Adenosine was much less effective, and GTP, UTP, CTP, and ITP were without effect. A similar increase in calcium current was observed when ATP was added in addition to a maximal stimulation by a beta-adrenergic agonist or after internal perfusion with cyclic AMP. However, this increase was preceded by a transient decrease whose origin could not be attributed to a P1-purinergic agonistic effect of ATP. The transient decrease was not elicited by adenosine or in a magnesium-free HEPES solution and was not suppressed after pertussis toxin treatment. This effect appeared related to the variations in the holding current also observed upon ATP application. Together with vasodilation, ATP and adenine compounds induced positive inotropy. The latter effect could be attributed in part to the increase in calcium current and was independent of cyclic AMP. Both effects are complementary with the beta-adrenergic stimulation and can help healthy cells to compensate the failing zone from which ATP could be released.

ATP and other adenine compounds increase mechanical activity and inositol trisphosphate production in rat heart.

1. The effects of adenosine 5'-triphosphate (ATP) and other adenine compounds were examined on rat papillary and right ventricular muscles in the presence of 10 microM-propranolol, 10 microM-atropine and 0.1 microM-prazosin or 10 microM-phentolamine. 2. Adenosine, adenosine 5'-monophosphate (AMP), adenosine 5'-diphosphate (ADP), ATP and alpha,beta-methylene ATP (APCPP) produced small positive inotropic effects, sometimes preceded by transient negative effects. 3. 8-Phenyltheophylline (8-PT), a P1-purinoceptor antagonist antagonized the negative effects and increased the positive inotropy induced by ATP and adenosine. 4. In the presence of APCPP, a P2-purinergic agonist, ATP had only negative inotropic effects. 5. Adenosine and ATP increased inositol 1, 4, 5- and inositol 1, 3, 4-trisphosphate as well as inositol mono- and bisphosphate formation. Maximal effects were obtained at concentrations of 0.5 mM. 6. APCPP increased inositol phosphate formation while 8-PT did not prevent the effects of adenosine and ATP. 7. It is suggested that P2-purinoceptor activation induces both a positive inotropy and an increase in inositol-lipid metabolism in rat ventricular muscles.

Sympathetic modulation of the effect of nifedipine on myocardial contraction and Ca current in the rat.

The regulation of cardiac L-type Ca2- current (Ica) and contraction by dihydropyridine antagonists and beta-adrenergic receptor agonists has been the subject of numerous studies over the last decade. However, little is known on the crosstalk between these two regulatory pathways. For instance, a fundamental question that remains unanswered is: does activation of the beta-adrenergic receptors modify the sensitivity of the myocardium to dihydropyridine agonists? To answer this question, we examined in the present study how activation of the beta-adrenergic receptors modifies the effects of nifedipine on the mechanical and energetic parameters of the isolated perfused rat heart. Activation of the beta-adrenergic receptors was achieved by perfusing the hearts with isoprenaline, a non-selective beta-adrenergic receptor agonist, and could be reduced by atenolol, a beta-adrenergic receptor antagonist. To examine possible alterations during hypertension in the sensitivity of the hearts to the drug, tested, the study was performed in both normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive animals (SHR). While 0.1 microM nifedipine reduced left ventricular pressure (LVP) by 36% and 34% in WKY and SHR rats, respectively, under basal conditions, its effects became negligible in both groups of rats after stimulation of the hearts with 0.1 microM isoprenaline. Addition of 1 microM atenolol in the presence of isoprenaline restored the inhibitory effect of nifedipine to control values in both WKY and SHR rats. Additional experiments were performed in isolated ventricular myocytes from WKY rats using the whole-cell patch-clamp technique. The inhibitory effects of 0.1 to 1 microM nifedipine were significantly larger on basal Ica than after the current had been previously elevated by 0.1 microM isoprenaline. Addition of 1 microM atenolol in the presence of isoprenaline partially restored the inhibitory effect of nifedipine on Ica. Our results demonstrate a reduced sensitivity of the heart muscle to nifedipine during activation of beta 1-adrenergic receptors. This effect is partly explained by a reduced inhibitory effect of nifedipine on Ic during activation of cAMP-dependent phosphorylation.