Investigating Majhool date (Phoenix dactylifera) consumption effects on fasting blood glucose in animals and humans.

OBJECTIVES: Majhool date (Phoenix dactylifera), renowned for its premium taste and texture, is extensively consumed in the Islamic world, particularly during Ramadan. Despite its popularity, concerns persist regarding its potential to induce diabetes in non-patients. This study aims to explore the diabetogenic effects of prolonged Majhool date (Phoenix dactylifera) consumption, the widely used fruit in the Islamic world, through animal experiments and human clinical data. METHODS: Medjool dates were processed into an ethanolic extract for the animal experiment. Then, 21 Balb/c mice received varying doses of the extract for one month. The fasting blood glucose levels were analyzed at the beginning and after one month of consumption of the Majhool date extract. For the clinical study, 387 healthy participants were recruited, with fasting blood glucose levels assessed before and after Ramadan, a period of heightened Majhool date consumption. RESULTS: all groups of the experimental animals exhibited a significant (p<0.05) weight increase after Majhool date consumption, while no significant (p>0.05) alteration in fasting blood glucose levels among groups. In addition, it was found that fasting blood glucose levels remained statistically unchanged (p>0.05) after heightened Majhool date consumption among humans. CONCLUSIONS: The study challenges the belief that Majhool date induces diabetes, supported by both animal and human data. Findings suggest that Majhool date consumption, even at higher doses, does not induce diabetes. Further investigations could explore the impact of other date varieties on the fasting blood glucose levels.

Molecular toxicological alterations in the mouse hearts induced by sub-chronic thiazolidinedione drugs administration.

Thiazolidinediones are well-known anti-diabetic drugs. However, they are not widely used due to their cardiotoxic effects. Therefore, in this study, we aimed to determine the molecular toxicological alterations induced in the mouse hearts after thiazolidinedione administration. Balb/c mice received doses clinically equivalent to those given to humans of the most commonly used thiazolidinediones, pioglitazone, and rosiglitazone for 30 days. After that, RNA samples were isolated from the hearts. The mRNA expression of cytochrome (cyp) p450 genes that synthesize the cardiotoxic 20-hydroxyeicosatetraenoic acid (20-HETE) in addition to 92 cardiotoxicity biomarker genes were analyzed using quantitative polymerase chain reaction array technique. The analysis demonstrated that thiazolidinediones caused a significant upregulation (p < 0.5) of the mRNA expression of cyp1a1, cyp4a12, itpr1, ccl7, ccr1, and b2 m genes. In addition, thiazolidinediones caused a significant (p < 0.05) downregulation of the mRNA expression of adra2a, bsn, col15a1, fosl1, Il6, bpifa1, plau, and reg3b genes. The most affected gene was itpr1 gene, which was upregulated by pioglitazone and rosiglitazone by sevenfold and 3.5-fold, respectively. In addition, pioglitazone caused significant upregulation of (p < 0.05) hamp, ppbp, psma2, sik1, timp1, and ucp1 genes, which were not affected significantly (p > 0.05) by rosiglitazone administration. In conclusion, this study showed that thiazolidinediones induce toxicological molecular alterations in the mouse hearts, such as the induction of cyp450s that synthesize 20-HETE, chemokine activation, inflammatory responses, blood clotting, and oxidative stress. These findings may help us understand the mechanism of cardiotoxicity involved in thiazolidinedione administration.