Fresh pomegranate juice ameliorates insulin resistance, enhances ß-cell function, and decreases fasting serum glucose in type 2 diabetic patients.

Although the effects of pomegranate juice (PJ) on type 2 diabetic (T2D) conditions have been reported, a clinical study focusing on the short-term effects on different diabetic variables is still needed. We hypothesized that PJ consumption by T2D patients could reduce their insulin-resistant state and decrease their fasting serum glucose (FSG) levels, 3 hours after juice ingestion. This study demonstrated the direct effect of fresh PJ on FSG and insulin levels in T2D patients. Blood samples from 85 participants with type 2 diabetes were collected after a 12-hour fast, then 1 and 3 hours after administration of 1.5 mL of PJ, per kg body weight. Serum glucose was measured based on standard methods using the BS-200 Chemistry Analyzer (Shenzhen Mindray Bio-Medical Electronics Co Ltd, Shenzhen, China). Commercially available immunoassay kits were used to measure human insulin. Generally, the results demonstrated decreased FSG, increased ß-cell function, and decreased insulin resistance among T2D participants, 3 hours after PJ administration (P < .05). This hypoglycemic response depended on initial FSG levels, as participants with lower FSG levels (7.1-8.7 mmol/L) demonstrated a greater hypoglycemic response (P < .05) compared with those who had higher FSG levels (8.8-15.8 mmol/L). The effect of PJ was also not affected by the sex of the patient and was less potent in elderly patients. In conclusion, this work offers some encouragement for T2D patients regarding PJ consumption as an additional contribution to control glucose levels.

Frequency of HLA-DQA1*0501 and DQB1*0201 alleles in patients with coeliac disease, their first-degree relatives and controls in Jordan.

BACKGROUND: The primary genetic marker associated with coeliac disease (CD) is the HLA-DQ2 molecule, encoded by the DQA1*0501 and DQB1*0201 genes. AIM: To investigate the frequency of HLA-DQA1*0501 and DQB1*0201 alleles in Jordanian patients with CD and their first-degree relatives. METHODS: An allele-specific DNA-based PCR-sequence-specific primer was used to investigate DQA1*0501 and DQB1*0201 alleles in 44 CD patients, 47 first-degree relatives and 53 healthy controls. RESULTS: The mean age of the patients at the time of diagnosis was 13.5 years (range 1-39) and at the time of the study was 19.3 years (range 5-42). The DQA1/B1 (0501; 0201) haplotype was present in 80% of patients and 66% of first-degree relatives compared with 32% of controls (p<0.0001 and <0.01, respectively). The remaining 20% of CD patients who were negative for the DQ2 molecule carried the DQB1*0201 allele only. A statistically significant difference was detected in the DQ2 hetero-dimer frequency between CD patients, their first-degree relatives and controls with a higher frequency in the patients group (p<0.001). CONCLUSION: The significant differences in the frequency of DQA1*0501, DQB1*0201 alleles in CD patients and their first-degree relatives compared with the control group demonstrated the important role of these alleles in the development of CD in the Jordanian population.

Does the plasma level of vitamins A and E affect acne condition?

BACKGROUND: Vitamin A and E are lipid soluble antioxidants that are necessary for our health. Deficiency in these vitamins can cause serious diseases. Administration of vitamin A and E to patients with acne was shown to improve their acne condition. AIMS: To test the relationship between plasma vitamin A and E levels and acne. METHODS: Plasma vitamin A and E concentrations were determined by high performance liquid chromatography in 100 newly diagnosed untreated patients with acne and were compared with those of 100 age-matched healthy controls. Patients were carefully graded using the Global Acne Grading System. RESULTS: We found that plasma vitamin A concentrations in patients with acne were significantly lower than those of the control group (336.5 vs. 418.1 mug/L, respectively) P = 0.007. We also found that plasma vitamin E concentrations in patients with acne were significantly lower than those of controls (5.4 vs. 5.9 mg/L) P = 0.05. In addition, we found that there is a strong relationship between decrease in plasma vitamin A levels and increase in the severity of acne condition. Patients with severe acne had significantly lower plasma concentrations of vitamins A and E than did those with lower acne grade and the age-matched healthy controls. DISCUSSION: Based on our results, we conclude that low vitamin A and E plasma levels have an important role in the pathogenesis of acne and in the aggravation of this condition.

Factors believed by Jordanian acne patients to affect their acne condition.

This study in Jordan described the pattern of acne in 166 untreated acne patients aged 13-42 years attending dermatology clinics and assessed patients' perceptions of factors that have an effect on their acne condition. Family history of acne was positive in 69.3% of acne patients. Emotional stress, hot weather and sweating were believed to be aggravating factors by acne patients of both sexes, and premenstrual factors and cosmetics were factors among women. Many acne patients believed that their acne was exacerbated by certain aspects of diet including nuts, chocolate, fatty food, fried food, eggs, cakes and biscuits, spices and coffee and tea.

Factors believed by Jordanian acne patients to affect their acne condition

This study in Jordan described the pattern of acne in 166 untreated acne patients aged 13-42 years attending dermatology clinics and assessed patients' perceptions of factors that have an effect on their acne condition. Family history of acne was positive in 69.3% of acne patients. Emotional stress, hot weather and sweating were believed to be aggravating factors by acne patients of both sexes, and premenstrual factors and cosmetics were factors among women. Many acne patients believed that their acne was exacerbated by certain aspects of diet including nuts, chocolate, fatty food, fried food, eggs, cakes and biscuits, spices and coffee and tea

Altered glutathione metabolism in oxaliplatin resistant ovarian carcinoma cells.

Elevation of glutathione (GSH) is commonly observed in cellular resistance to a number of anticancer agents. Most frequently reported change in GSH metabolism that is associated with the elevated GSH levels is increased mRNA expression and activity of gamma-glutamyl cysteine synthetase (gamma GCS), the first enzyme of the GSH biosynthetic pathway. We have isolated sublines of the A2780 ovarian carcinoma cell line (C10 and C25) that are 8- and 12-fold resistant to oxaliplatin by repeatedly exposing the cells to increasing concentrations of the platinum agent. The GSH levels in C10 and C25 cell sublines are 3.1- and 3.8-fold higher than the parent A2780 cell line. The mRNA levels and activities for gamma GCS and that for gamma-glutamyl transpeptidase (gamma GT), the GSH salvage pathway enzyme, were measured in these cells. The mRNA for gamma GT and gamma GCS were measured by RT-PCR, with quantitation of the PCR product by HPLC; mRNA levels are expressed as ratios to beta-actin mRNA, used as an endogenous standard. GSH and gamma GCS activity were measured by HPLC assays and gamma GT activity by a colorimetric assay. The increase in GSH in C10 and C25 was associated with an elevation in gamma GT mRNA (2.5- and 8-fold) and gamma GT activity (2.7- and 2.8-fold). No changes were observed in gamma GCS mRNA levels or activity. The data indicate that alterations in GSH metabolism leading to elevations in cellular GSH in A2780 ovarian carcinoma cells selected for low levels of resistance to oxaliplatin are mediated by gamma GT, the "salvage' pathway, rather than an increase in GSH biosynthesis.

Induction of gamma-glutamyl transpeptidase mRNA by platinum complexes in a human ovarian carcinoma cell line.

Elevation of glutathione (GSH) is widely observed in cellular resistance to platinum agents. Our previous studies have shown that sublines of human ovarian carcinoma cell line A2780, which exhibited low levels of resistance to oxaliplatin, showed elevated steady state levels of mRNA and activity of gamma-glutamyl transpeptidase (gamma-GT, EC 2.3.2.2), but not of gamma-glutamylcysteine synthetase (gamma-GCS, EC 6.3.2.2) [El-akawi et al., Cancer Lett. 105:5-14; 1966]. To understand this phenomenon better, we have studied the effect of single exposures of oxaliplatin or cisplatin on the mRNA expression of gamma-GT and gamma-GCS in A2780 cells. The mRNAs of gamma-GT and gamma-GCS were measured by reverse transcriptase PCR, with quantitation of the PCR product by HPLC; mRNA levels are expressed as ratios to beta-actin mRNA, used as an endogenous standard. GSH was measured by HPLC. The gamma-GT activity was measured by a colorimetric assay. Single exposures of cells to oxaliplatin induced a time- and concentration-dependent increase in the mRNA of gamma-GT, but not of gamma-GCS. Cisplatin also induced an elevation in gamma-GT mRNA, but to a lower degree. The gamma-GT enzyme activity increased corresponding to the elevation in mRNA expression. The gamma-GT-induced cells showed an increase in cellular GSH when incubated in medium containing GSH. The data suggest that a) single, brief exposures to pharmacologically relevant concentrations of platinum complexes induce elevation in mRNA of gamma-GT, b) elevation in gamma-GT mRNA translates into elevated gamma-GT activity and increase in GSH salvage, and c) the degree of induction of gamma-GT mRNA differs between platinum complexes.

Rat liver cytosolic retinal dehydrogenase: comparison of 13-cis-, 9-cis-, and all-trans-retinal as substrates and effects of cellular retinoid-binding proteins and retinoic acid on activity.

A basic pI retinal dehydrogenase has been purified recently that accounts for approximately 90% of the all-trans-retinal dehydrogenase activity of rat liver cytosol. In this work, we show that this enzyme also accounts for approximately 90% of the 9-cis-retinal dehydrogenase activity of rat liver cytosol. The partially-purified enzyme displayed allosteric kinetics for 9-cis-retinal [K0.5 = 5.2 microM, Hill coefficient = 1.4, Vmax = 7.85 nmol min-1 (mg of protein)-1] with the ratio Vmax/K0.5 = 1.5. The latter is similar to that of 2.1 for all-trans-retinal [K0.5 = 1.6 microM, Hill coefficient = 1.4, Vmax = 3.4 nmol min-1 (mg of protein)-1]. Competition between all-trans- and 9-cis-retinal occurred only when micromolar concentrations of both were present, indicating that the dehydrogenase could catalyze both all-trans- and 9-cis-retinoic acid syntheses simultaneously at the nanomolar amounts of the retinals that are likely to occur physiologically. Although reactions of all-trans- and 9-cis-retinoids were catalyzed with similar efficiencies, 13-cis-retinal was not an efficient substrate. This retinal dehydrogenase was not feedback-inhibited by all-trans- or 9-cis-retinoic acid, nor by holocellular retinoic acid-binding protein, but was stimulated modestly by apocellular retinoic acid-binding protein, an effect not observed in the presence of cellular retinol-binding protein. These data indicate that products, via feedback inhibition, do not regulate retinoic acid synthesis by this dehydrogenase. This dehydrogenase may serve as a common enzyme in the conversion of all-trans- and 9-cis-retinal into their acids.