Changes in Body Composition and Mitochondrial Nucleic Acid Content in Patients Switched from Failed Nucleoside Analogue Therapy to Ritonavir‐Boosted Indinavir and Efavirenz

Abstract

This regimen was associated with statistically significant but clinically modest increases in peripheral fat, visceral fat, and mitochondrial nucleic acid content. A predominantly adverse metabolic profile developed.

Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohnʼs disease

“…In comparison, antiretroviral HIV therapy, which is also known to induce fat redistribution, caused in 1 report a 9% increase in total abdominal fat after 48 weeks of treatment. 31 Similar to antiretroviral HIV therapy, the increase in abdominal fat mass during infliximab therapy was homogeneous, as a broadly similar increase was observed in subcutaneous and visceral fat. This may be due to a similar expression level of TNF receptors in subcutaneous and visceral adipose tissues.…”

Adipocyte dysfunction in response to antiretroviral therapy: clinical, tissue and in-vitro studies

“…Body-fat tissue abnormalities are exacerbated when treatments include the first-generation NRTIs or protease inhibitors [15 ,18,19]. Lipoatrophy in the face and extremities has been linked repeatedly to the use of stavudine (and to a lesser extent zidovudine) among NRTIs [20,21] and increases with long-term exposure [22 ]. Protease inhibitors have mainly been associated with central fat accumulation along with insulin resistance.…”

Lipodystrophy in HIV 1-infected patients: lessons for obesity research

“…21 Similar findings were reported when a stavudine-based regime was replaced with a treatment containing protease inhibitors and efavirenz, an NNRTI less prone to causing mitochondrial toxicity. 22 Treatment of rat with the NRTI zidovudine causes mtDNA depletion and, moreover, several studies have indicated that anti-retroviral drugs that cause mtDNA depletion also impair adipocyte differentiation in cell culture, 7 and treatment of adipocyte cell cultures with uridine, which averts mitochondrial dysfunction, prevents NRTI-induced impairment in adipocyte differentiation 23 and ameliorates lipodystrophy 'in vivo'. 24 Therefore, extensive studies on mitochondria and HALS have demonstrated that mitochondrial disturbances in adipose tissue are capable of eliciting profound effects in adipose tissue biology and appear to promote lipoatrophy.…”