METHODS: The literature search was implemented in four following databases: Web of Science, Scopus, PubMed/Medline, and Google Scholar, thus, determining studies that measured the effects of walnut consumption on adiponectin, leptin, and glycemic biomarkers levels from 2004 up to December 2019.
RESULTS: Fourteen trials were include in the meta-analysis, with an intervention period ranging from 5 weeks to 12 months.Walnut intake increased leptin (weighted mean difference (WMD): 2.502 ng/mL; 95 % CI: 2.147-2.856, p leptin and adiponectin levels but does not improve glycemic biomarkers.
METHODOLOGY: This study comprised of 249 participants (148 overweight/ obese as a case group and 101 lean participants as controls). The PCR-RFLP technique was performed to distinguish the genotype distribution of Leptin gene polymorphisms. The allele and genotype frequencies were assessed for single and haplotype analyses.
RESULT: Single association analysis of G2548A (P=0.74), A19G (P=0.38), and H1328080 (P=0.56) polymorphisms yielded no statistically significant association. However, haplotype association analysis showed a suggestive indication of AAG haplotype (G2548A, H1328080, and A19G sequence) with susceptibility effect towards obesity predisposition [P=0.002, OR=8.897 (1.59-9.78)].
CONCLUSION: This data on single and haplotype might disclose the preliminary exposure and pave the way for the obesity development with an evidence of revealed susceptibility to obesity.
OBJECTIVE: In the present study, bioassay-guided screening technique was employed to identify the best AP extract in the management of MetS, PCa, and MetS-PCa co-disease in vitro.
METHODS: Five AP extracts by different solvent systems; APE1 (aqueous), APE2 (absolute methanol), APE3 (absolute ethanol), APE4 (40% methanol), and APE5 (60% ethanol) were screened through their phytochemical profile, in-vitro anti-cancer, anti-obese, and anti-hyperglycemic properties. The best extract was further tested for its potential in MetS-induced PCa progression.
RESULTS: APE2 contained the highest andrographolide (1.34 ± 0.05 mg/mL) and total phenolic content (8.85 ± 0.63 GAE/gDW). However, APE3 has the highest flavonoid content (11.52 ± 0.80 RE/gDW). APE2 was also a good scavenger of DPPH radicals (EC50 = 397.0 µg/mL). In cell-based assays, among all extracts, APE2 exhibited the highest antiproliferative activity (IC50 = 57.5 ± 11.8 µg/mL) on DU145 cancer cell line as well as on its migration activity. In in-vitro anti-obese study, all extracts significantly reduced lipid formation in 3T3-L1 cells. The highest insulin-sensitizing and -mimicking actions were exerted by both APE2 and APE3. Taken together, APE2 showed collectively good activity in the inhibition of PCa progression and MetS manifestation in vitro, compared to other extracts. Therefore, APE2 was further investigated for its potential to intervene DU145 progression induced with leptin (10-100 ng/mL) and adipocyte conditioned media (CM) (10% v/v). Interestingly, APE2 significantly diminished the progression of the cancer cell that has been pre-treated with leptin and CM through cell cycle arrest at S phase and induction of cell death.
CONCLUSION: In conclusion, AP extracts rich with andrographolide has the potential to be used as an alternative to ameliorate PCa progression induced by factors highly expressed in MetS.