Homocysteine, cysteine, folate and vitamin B12 status in type 2 diabetic patients with chronic kidney disease

Abstract

Hyperhomocysteinemia (hHcy) is a risk\ud factor in the progression of chronic kidney disease (CKD).\ud In type 2 diabetes (T2D), hHcy is strongly associated with\ud increased risk of cardiovascular disease. Vitamin B12 and\ud folic acid supplementation have been reported to lower\ud homocysteine (tHcy) levels, but no data on plasma tHcy,\ud cysteine (Cys), folate and vitamin B12 levels in T2D-CKD\ud patients are reported.\ud Procedures tHcy and Cys levels were analyzed in 178\ud T2D-CKD patients by high performance liquid chromatography\ud (HPLC) with fluorescence detection. In addition,\ud we determined folate and vitamin B12 levels using a\ud chemiluminescence method.\ud Results tHcy and Cys levels were increased in T2D\ud patients, and this rise positively correlated with the CKD\ud stage (P\0.001). Folate levels were comparable to controls\ud at various CKD stages, whereas vitamin B12 levels\ud were lower, except at stage IV. We did not find any\ud correlation between B-vitamins and levels of tHcy and Cys,\ud regardless of the CKD stage.\ud Conclusions This is the first study reporting tHcy, Cys\ud and B-vitamins status in T2D-CKD patients. Although\ud limited to our cohort of 178 patients, our findings could be\ud helpful in clarifying the conflicting literature regarding\ud B-vitamins supplementation. Further studies are necessary\ud before any Hcy-lowering therapy can be safely established\ud in T2D-CKD subjects

Oleuropein, a Bioactive Compound from Olea europaea L., as a Potential Preventive and Therapeutic Agent in Non-Communicable Diseases

“…Di Daniele et al [55] demonstrated that the Italian MD in nephropatic patients could be a useful tool in the treatment of cardiovascular comorbidity related to renal dysfunction, causing a significant decrease in serum homocysteine (Hcy), dependant on a methylenetetrahydrofolate reductase genotype. In fact, Hcy, during the autoxidation process, induces impairment of the endothelium by producing ROS, with consequent involvement in atherosclerosis [56,57]. All these studies support that adherence to the MD with EVOO can modify inflammation, regardless of shared genetic and environmental factors.…”

Metabolomic analysis of obesity, metabolic syndrome, and type 2 diabetes: amino acid and acylcarnitine levels change along a spectrum of metabolic wellness

“…1). Cystine levels could be elevated as a result of increased oxidative stress, or very early renal dysfunction (Buckley & Milligan, 1978; Hargrove & Wichman, 1987; Wijekoon, Brosnan & Brosnan, 2007; Pastore et al, 2015). Cysteine inhibits tyrosine aminotransferase activity, and can lead to an increased plasma tyrosine level (Buckley & Milligan, 1978; Hargrove & Wichman, 1987).…”

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

“…Conversely, the species found to be decreased in CKD are among those that strengthen gut barrier function [16,36,37]; produce anti-inflammatory [46,71,73,109], NO [16,47], CDCA, UDCA [50,[83][84][85], GABA [60,61,110], Ach [65,107,108], and the vitamin B complex [17, 52-54, 81, 82]; increase the production of gut hormones with anti-inflammatory properties [57][58][59][76][77][78][79]; increase anti-inflammatory vagal activity [90,93,97]; and decrease pro-inflammatory renal sympathetic activity. Interestingly, CKD is associated with gut barrier dysfunction, an increase in uremic toxins [101], elevated renal sympathetic activity [111], lower group B vitamin levels [112][113][114] and NO [115], and a reduction in vagal activity [116], which may stem from the gut dysbiosis found in patients with CKD. Therefore, we can suggest that a healthy gut microbiota can protect from CKD, whereas gut dysbiosis takes part in the development and progression of CKD through a number of pathways that manipulate host inflammatory activity.…”