Plasma levels of lipopolysaccharide correlate with insulin resistance in HIV patients

Abstract

BackgroundIn HIV patients using HAART insulin resistance is a central pathophysiological condition that can contribute to the development of diabetes and cardiovascular complications. To examine the role of adipocyte hormones and LPS in insulin resistance in HIV patients, we investigated the role of adiponectin, leptin, visfatin and LPS levels in the insulin resistance of HIV-infected patients treated with HAART.MethodsThis study included 67 HIV positive individuals on HAART and ten healthy controls. All participants performed plasma or serum levels of glucose; insulin; lipids, visfatin, leptin, adiponectin, and LPS. The homeostasis model assessment (HOMA-IR), was used to estimate insulin resistance.ResultsThe levels of visfatin, leptin and adiponectin were similar between controls and HIV patients. However, circulating levels of LPS were higher in HIV patients on HAART than in controls. There was a positive correlation between LPS and TG (r = 0.49, p = 0.0001), between LPS and TG/HDL (r = 0.50, p = 0.0001), between LPS and insulin (r = 0.52, p = 0.0003), and between LPS and HOMA-IR (r = 0.52, p = 0.0005), in HIV patients.ConclusionsOur results showed a clear correlation between plasma LPS and markers of insulin resistance, suggesting a relationship between LPS levels and metabolic alterations, particularly affecting lipids and insulin resistance in HIV patients.

Gut Bacterial Communities in HIV-Infected Individuals with Metabolic Syndrome: Effects of the Therapy with Integrase Strand Transfer Inhibitor-Based and Protease Inhibitor-Based Regimens

“…Increased concentrations of plasmatic LPS have been observed in HIV-infected patients, even on ART. Plasma LPS has been shown to have a significant positive correlation with triglycerides and markers of insulin resistance as well [96]. Interestingly, we also found pathways related to arginine degradation in the INSTI + MetS group, which have also been related to the pro-inflammatory state elicited by the LPS-induced IL-6 response (HISDEG-PWY, ARGDEG-PWY, ORNARGDEG-PWY) [97].…”

Oligosaccharides derived from Lycium barbarum ameliorate glycolipid metabolism and modulate the gut microbiota community and the faecal metabolites in a type 2 diabetes mouse model: metabolomic bioinformatic analysis

“…The LBO-M group may provide Bacteroidetes with full utilization of carbohydrates and a more superior growth environment than Firmicutes and alleviate the obesity caused by the pathogenesis of T2D inflammation and hyperglycemia. 58 Several pieces of evidence suggest that disturbances in the balance of the gut microbiome may straightway give rise to increased intestinal permeability, which may be associated with the extravasation of Gram-negative bacterium derived lipopolysaccharide from the gut into the bloodstream, rendering individuals in an inflammatory state and prone to the formation of insulin resistance, 59,60 thus also confirming that the gut microbiome has an essential role in the pathogenesis of diabetes. 56 The abundance of Proteobacteria, which belong to Gram-negative bacteria, has been verified to increase in the gut of T2D mice.…”

Distinct Plasma Metabolomic and Gut Microbiome Profiles After GDM Diet Treatment: Implications for Personalized Dietary Interventions

“…A higher abundance of P. copri is associated with worse insulin resistance and glycemic control both in adults with and without T2D [51][52][53] through the biosynthesis of branched-chain amino acids and LPS by the taxon [51,52]. Both branched-chain amino acids [54] and LPS [55,56] are implicated in the development and maintenance of insulin resistance by enhancing inflammation and lipid accumulation in various tissues [57,58]. While CONV diet was not associated with changes in branched-chain amino acid levels, KEGG gene pathways revealed an enrichment in amino acid metabolism and inflammatory pathways such as antimicrobial resistance and LPS biosynthesis, that potentially impact gut function in women with GDM on higher fat diets.…”