Olive tree (Olea europaea L.) leaves have been widely used in traditional remedies in European and Mediterranean countries as extracts, herbal teas, and powder. They contain several potentially bioactive compounds that may have hypoglycemic properties. To examine the efficacy of 500 mg oral olive leaf extract taken once daily in tablet form versus matching placebo in improving glucose homeostasis in adults with type 2 diabetes (T2DM). In this controlled clinical trial, 79 adults with T2DM were randomized to treatment with 500 mg olive leaf extract tablet taken orally once daily or matching placebo. The study duration was 14 weeks. Measures of glucose homeostasis including Hba1c and plasma insulin were measured and compared by treatment assignment. In a series of animal models, normal, streptozotocin (STZ) diabetic, and sand rats were used in the inverted sac model to determine the mechanism through which olive leaf extract affected starch digestion and absorption. In the randomized clinical trial, the subjects treated with olive leaf extract exhibited significantly lower HbA1c and fasting plasma insulin levels; however, postprandial plasma insulin levels did not differ significantly by treatment group. In the animal models, normal and STZ diabetic rats exhibited significantly reduced starch digestion and absorption after treatment with olive leaf extract compared with intestine without olive leaf treatment. Reduced digestion and absorption was observed in both the mucosal and serosal sides of the intestine. Though reduced, the decline in starch digestion and absorption did not reach statistical significance in the sand rats. Olive leaf extract is associated with improved glucose homeostasis in humans. Animal models indicate that this may be facilitated through the reduction of starch digestion and absorption. Olive leaf extract may represent an effective adjunct therapy that normalizes glucose homeostasis in individuals with diabetes.
An increase in endogenous androgen production has been observed following long-term physical training and the beneficial effects of training have been attributed in part to this phenomenon. Other investigators, however, found, in contrast lower testosterone levels in trained compared with untrained subjects. The purpose of the present study was to follow the long-term changes in total testosterone (T) and cortisol (C) levels in intensely training individuals. The changes in the body's anabolic state, induced by intense long-term physical training, were determined using the plasma resting T/C ratio. T and C levels of 35 young untrained subjects were measured at 6 week intervals during 18 weeks of strenuous physical training. All samples were drawn within one half hour of awaking (05.30-06.00). Mean serum T levels increased significantly at 6 weeks (28.7%, p less than 0.02) and decreased significantly at 12 weeks (20.6%, p less than 0.02), but did not differ at 18 weeks compared with levels before training was commenced (mean +/- SE, 16.9 +/- 0.2, 21.8 +/- 0.3, 12.8 +/- 0.2 and 17.3 +/- 0.2 nmol/l at 0, 6, 12, and 18 weeks, respectively). Mean serum C was increased significantly (21.3%, p less than 0.005) at 18 weeks (463.5 +/- 19.3, 507.7 +/- 22.1, 480.1 +/- 19.3, and 565.6 +/- 22.1 nmol/l). T/C ratio decreased significantly after 12 and 18 weeks of training. Our results do not support an association between reduced total testosterone levels and prolonged training. However, hypercorticolism with a relative catabolic state may occur.
Nearly 50 medications have been implicated as inducing hypomagnesaemia, sometimes based on insufficient data regarding clinical significance and frequency of occurrence. In fact, clinical effects attributed to hypomagnaesemia have been reported in only 17 of these drugs. A considerable amount of literature relating to individual drugs has been published, yet a comprehensive overview of this issue is not available and the hypomagnesaemic effect of a drug could be either overemphasised or under-rated. In addition, there are neither guidelines regarding treatment, prevention and monitoring of drug-induced hypomagnesaemia nor agreement as to what serum level of magnesium may actually be defined as 'hypomagnesaemia'. By compiling data from published papers, electronic databases, textbooks and product information leaflets, we attempted to assess the clinical significance of hypomagnesaemia induced by each drug. A practical approach for managing drug-induced hypomagnesaemia, incorporating both published literature and personal experience of the physician, is proposed. When drugs classified as inducing 'significant' hypomagnesaemia (cisplatin, amphotericin B, ciclosporin) are administered, routine magnesium monitoring is warranted, preventive treatment should be considered and treatment of hypomagnesaemia should be initiated with or without overt clinical manifestations. In drugs belonging to the 'potentially significant' category, among which are amikacin, gentamicin, laxatives, pentamidine, tobramycin, tacrolimus and carboplatin, magnesium monitoring is justified when either of the following occurs: clinical manifestations are apparent; persistent hypokalaemia, hypocalcaemia or alkalosis are present; other precipitating factors for hypomagnesaemia coexist; or treatment is with more than one potentially hypomagnesaemic drug. No preventive treatment is required and treatment should be initiated only if hypomagnesaemia is accompanied by symptoms or clinically significant relevant laboratory findings. In those drugs whose hypomagnesaemic effect is labelled as 'questionable', including furosemide and hydrochlorothiazide, routine monitoring and treatment are not required.
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