An association between adropin hormone and total testosterone in obese men: a case-control study.

BACKGROUND: Obesity is associated with low testosterone levels that could be caused by many mechanisms. Adropin, a peptide hormone, its levels are decreased in obesity and its receptors are expressed in the hypothalamus, the pituitary gland, and the testis. Adropin association to total testosterone in obese men is not detected yet. This study tries to find out possible associations between serum levels of adropin, adiponectin, total testosterone, and lipid profile in obese men. METHODS: Serum levels of adropin, adiponectin, total testosterone, and lipid profile parameters were measured in 43 obese men and 40 age-matched normal-weight men. RESULTS: Adropin, adiponectin, and testosterone levels were significantly lower in obese men versus normal-weight men. In all participants, positive correlations between adropin, adiponectin, and total testosterone were detected. Adropin is considered a predictor risk factor for testosterone. CONCLUSIONS: This study suggests a possible causal relationship between adropin and total testosterone which needs further investigation. TRIAL REGISTRATION: Clincialtrials.gov NCT03724825 , registered October 30th, 2018.

Protective and antioxidant effects of copper-nicotinate complex against glycerol-induced nephrotoxicity in rats.

Copper-nicotinate complex (CNC) has antioxidant activities through scavenging of free radicals formed inside the body. CNC also has anti-tumor and anti-inflammatory activities. The current study was designed to determine the effect of glycerol on rat kidney function and oxidative stress as well as, the potential nephroprotective effects of CNC. Forty male Wistar rats were randomly allocated into four equal groups. The groups of rats were as follows: GI was kept under normal control conditions; GII was orally given CNC at a dose of 0.043 mg kg-1 body weight (BW), three times/week for 4 weeks; GIII was administered glycerol (topical application) at a dose of 3.15 ml kg-1 BW daily for 4 weeks; and GIV was given CNC and glycerol with the same dose and route. The results revealed that CNC improves the renal dysfunctions induced by glycerol by recovering the levels of urea and creatinine to normal, as well as through the antioxidant status manifested by the normalization of catalase, superoxide dismutase, reduced glutathione, and malondialdehyde levels. Moreover, by its effect as an anti-oxidant, CNC reduces the effect of glycerol on the kidney by decreasing the fibrosis, degenerative changes and necrotic changes in the renal tubules. In conclusion, CNC could alleviate the side effects that might be caused by glycerol.

Hepatoprotective and immunomodulatory effects of copper-nicotinate complex against fatty liver in rat model.

AIM: The current study was designed to evaluate the potential hepatoprotective and immunomodulatory effects of copper-nicotinate complex (CNC) against methionine- and choline-deficient diet (MCDD)-induced fatty liver in rats. MATERIALS AND METHODS: Forty male Wistar rats were randomly allocated into one of four equal-sized groups (G1-G4). The G1 group was fed a balanced diet and kept under normal conditions; the G2 group received CNC orally at a dose of 0.043 mg/kg body weight, 3 times/week for 4 weeks, and a balanced diet; the G3 group was fed an MCDD for 4 weeks; and the G4 group was fed an MCDD and administered CNC at the same dose and route as G2. Blood samples were collected for the determination of serum enzyme activity. After 4 weeks of treatment, liver specimens were collected for the evaluation of the oxidative/antioxidative markers, cytokine gene expression, and histopathological examination. RESULTS: CNC improved MCDD-induced liver dysfunctions by recovering serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities to their normal levels. The glutathione (GSH) level and superoxide dismutase (SOD) activity significantly decreased, while lipid peroxidation (as reflected by malondialdehyde [MDA]) markedly increased in the liver tissue of the MCDD group. After cotreatment with MCDD and CNC, the GSH level and SOD activity markedly increased and the MDA level significantly decreased to return to normal levels. After cotreatment with MCDD and CNC, significant downregulation of the mRNA expression of hepatic interleukin (IL)-1ß, IL-4, macrophage inflammatory protein-1α, and monocyte chemoattractant protein-1 genes was found. Moreover, CNC reduced fatty liver complications by reducing the number of hepatic vacuolations, degenerative changes in the hepatocytes, and hemorrhage. CONCLUSION: CNC has the potential to limit tissue injury and possibly prevent the progression to severe liver disease caused by an MCDD.

Improving hepatic mitochondrial biogenesis as a postulated mechanism for the antidiabetic effect of Spirulina platensis in comparison with metformin.

Various nutritional and medicinal potencies have been accredited to metabolites from the cyanobacteria, Spirulina platensis (Arthrospira platensis) sp. Hence, our study was designed to examine whether the Spirulina supplementation would possess beneficial effects in type 2 diabetes mellitus (T2DM) in comparison with metformin. High-fat diet/low-dose streptozotocin (HFD/STZ) model was adopted and the diabetic rats were orally treated with metformin (200 mg/kg) or Spirulina (250 or 500 or 750 mg/kg) for 30 days. Spirulina ameliorated the HFD/STZ-induced elevation of fasting blood glucose, insulin, and hepatic enzymes. Moreover, Spirulina successfully rectified disrupted serum lipid profile and exhibited an anti-inflammatory effect via tumor necrosis factor-α and adiponectin modulation. On the molecular level, Spirulina reduced the expression of hepatic sterol regulatory element binding protein-1c (SREBP-1c), confirming its lipotropic effect. Furthermore, Spirulina amended compromised hepatic mitochondrial biogenesis signaling by significantly increasing peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), mitochondrial transcription factor A (Tfam), and mitochondrial DNA (mtDNA) copy number. On almost all parameters, the highest dose of Spirulina showed the best effects, which were comparable to that of metformin. To our knowledge, our study is the first to attribute the various aspects of the effect of Spirulina to the SREBP-1c and PGC-1α/Tfam/mtDNA pathways in liver. The present results clearly proved that Spirulina modulated glucose/lipid profile and exhibited prominent anti-inflammatory properties through SREBP-1c inhibition and hepatic mitochondrial biogenesis enhancement. Thus, Spirulina can be considered as an add-on to conventional antidiabetic agents and might influence the whole dynamics of the therapeutic approaches in T2DM.

Vitamin C and E chronic supplementation differentially affect hepatic insulin signaling in rats.

AIM: Vitamin C and vitamin E supplementations and their beneficial effects on type 2 diabetes mellitus (T2DM) have been subjected to countless controversial data. Hence, our aim is to investigate the hepatic molecular mechanisms of any diabetic predisposing risk of the chronic administration of different doses of vitamin E or vitamin C in rats. MAIN METHODS: The rats were supplemented with different doses of vitamin C or vitamin E for eight months. KEY FINDINGS: Vitamin C and vitamin E increased fasting blood glucose, insulin, and homeostasis model assessment index for insulin resistance (HOMA). Vitamin C disrupted glucose tolerance by attenuating upstream hepatic insulin action through impairing the phosphorylation and activation of insulin receptor and its subsequent substrates; however, vitamin E showed its effect downstream insulin receptor in the insulin signaling pathway, reducing hepatic glucose transporter-2 (GLUT2) and phosphorylated protein kinase (p-Akt). Moreover, both vitamins showed their antioxidant capabilities [nuclear factor-erythroid-2-related factor 2 (Nrf2), total and reduced glutathione] and their negative effect on Wnt pathway [phosphorylated glycogen synthase kinase-3ß (p-GSK-3ß)], by altering the previously mentioned parameters, inevitably leading to severe reduction of reactive oxygen species (ROS) below the physiological levels. SIGNIFICANCE: In conclusion, a detrimental effect of chronic antioxidant vitamins supplementation was detected; leading to insulin resistance and impaired glucose tolerance obviously through different mechanisms. Overall, these findings indicate that the conventional view that vitamins promote health benefits and delay chronic illnesses and aging should be modified or applied with caution.