Test of insulin resistance in nondiabetic and streptozotocin-induced diabetic rats using glycosylated hemoglobin test and other interventions.

Type 2 diabetes is common globally. Pioglitazone (PGZ) is an oral TZD antidiabetic, whereas chromium-picolinate (Cr-PL) and Cr-glucose tolerance factor (Cr-GTF) are useful type 2 diabetes mellitus (T2DM) supplements. Cr-PL/GTF antioxidants cure T2DM. They may fail in diabetes with or without insulin-sensitizing medications. It examined how Cr-PL, Cr-GTF, PGZ, and their combination affected glucose, glycosylated hemoglobin, insulin, and HOMA-IR. Sixty-three adult Sprague-Dawley rats (220-300 g) were selected, and nine rats were randomly assigned to a normal nondiabetic group. In contrast, 54 rats were randomly split into 9 rats per each of the 6 major groups and injected intraperitoneally with 40 mg/kg STZ to induce T2DM. Rats were administered PGZ = 0.65 mg/kg (rat weight)/day, Cr-PL = 1 mg/kg, Cr-GTF = 1 mg/kg, and their combinations (PGZ + Cr-PL and Cr-GTF) daily for 6 weeks per intervention. The PGZ + Cr-PL and PGZ + Cr-GTF groups had substantially lower insulin levels than the PGZ group (13.38 ± 0.06, 12.98 ± 0.19 vs. 14.11 ± 0.02, respectively), with the PGZ + Cr-GTF group having the lowest insulin levels (12.98 ± 0.19 vs. 14.11 ± 0.02, 13.38±0.06, respectively). Intervention substantially reduced HOMA-IR in the PZ + Cr-PL and PZ + Cr-GTF groups compared to PGZ (7.49 ± 0.04, 6.69 ± 0.11 vs. 8.37 ± 0.04, respectively). This research found that combining PGZ with Cr-GTF resulted in considerably lower HOMA-IR levels than the PGZ and Cr-PL groups (6.69 ± 0.11 vs. 8.37 ± 0.04, 7.49 ± 0.04, respectively). Both Cr-PL and Cr-GTF may control T2DM. Both Cr complexes improved T2DM biomarkers more than the control diabetic group without medication. PGZ alone and PGZ + Cr-PL had less pharmacological synergy than Cr-GTF and PGZ in altering insulin and HOMA-IR blood levels. These encouraging discoveries need more study.

An additional marker for sperm DNA quality evaluation in spermatozoa of male partners of couples undergoing assisted reproduction technique (IVF/ICSI): Protamine ratio.

The aim of this study was to evaluate the relationship between the protamine ratio (P1/P2), DNA fragmentation of spermatozoa and protamine deficiency. Patients were grouped into fertile (G1; n = 151) and sub-fertile (G2; n = 121). DNA fragmentation in spermatozoa was analysed by a TUNEL assay (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling), and the protamination was determined by CMA3 staining, while Western blot was used to measure protamine P1 and P2. While sperm DNA fragmentation (SDF) and protamine ratio were significantly elevated in G2 compared with G1 (12.31 ± 7.01% vs. 17.5 ± 9.5%; p = .001) and (0.91 ± 0.43 vs. 0.75 ± 0.42; p = .003); respectively, the CMA3 positive showed no difference at all between G1 and G2. In G1, the CMA3 positive correlated negatively with the P1/P2 ratio and SDF (r = -.586, r = -.297; p = .001 respectively). In contrast, the protamine ratio correlated positively with SDF (r = .356; p = .001). In G2, no correlation was observed between CMA3 positive, SDF and the P1/P2 ratio but the P1/P2 ratio showed a positive correlation with SDF (r = .479; p = .001). In conclusion, the spermatozoa DNA deterioration was closely associated with abnormal protamination but showed an association with the protamine ratio, more than with CMA3 positive. Therefore, for the evaluation of DNA damage in spermatozoa, the P1/P2 ratio might act as an additional biomarker.

The status of global DNA methylation in the spermatozoa of smokers and non-smokers.

RESEARCH QUESTION: Does regular smoking affect semen quality and the levels of DNA methylation in mature human spermatozoa? DESIGN: Spermatozoa from 109 men were evaluated (55 smokers and 54 non-smokers). DNA was extracted from purified spermatozoa, and DNA methylation was quantified by enzyme-linked immunosorbent assay (ELISA). RESULTS: Global DNA methylation of non-smokers is significantly lower (P < 0.001) than that of smokers (4.85 ±â€¯2.72 and 7.08 ±â€¯1.77 ng/µl, respectively). Moreover, the mean global DNA methylation levels were significantly correlated (r = 0.22;P = 0.02) with non-condensed chromatin in the spermatozoa. Levels of non-condensed chromatin were significantly higher (P < 0.001) in smokers (29.75 ±â€¯9.38%) compared with non-smokers (20.96 ±â€¯11.31%). Furthermore, global sperm DNA methylation was negatively correlated with high significance (P < 0.010) with sperm: count (r = -0.27), motility (r = -0.30) and vitality (r = -0.26). CONCLUSION: Smoking interferes with DNA methylation. Also, DNA methylation is significantly correlated with sperm parameters and sperm non-condensed chromatin. These data emphasize another detrimental effect of smoking on male fertility. DNA methylation may, therefore, be considered as a fertility marker in men.