HIV protease inhibitors and insulin resistance: lessons from in-vitro, rodent and healthy human volunteer models
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PURPOSE OF REVIEW: Although the use of HIV protease inhibitors is linked to the development of insulin resistance and other metabolic changes that greatly increase the risk for cardiovascular disease, the molecular mechanisms responsible remain incompletely understood. This review summarizes recent advances that have been made in understanding the relative contributions of individual protease inhibitors to both acute and chronic insulin resistance together with newly identified cellular mediators. RECENT FINDINGS: Individual protease inhibitors, alone and in combination, have differing propensities to induce insulin resistance, reflecting relative differences in both affinities for identified molecular targets and pharmacokinetic profiles. Several of the most recent protease inhibitors approved for clinical use or in development appear to be less likely to induce insulin resistance. In addition to direct effects on glucose transporter-4 activity, induction of oxidative stress, proteosome inhibition, alteration of adipokine levels, and changes in suppressors of cytokine signaling-1 have been implicated. SUMMARY: A better understanding of the propensity of individual HIV protease inhibitors to produce insulin resistance will allow the tailoring of individual treatment plans based upon overall risk for diabetes. The elucidation of the molecular mechanisms for alterations in glucose homeostasis will facilitate the development of newer generations of HIV protease inhibitors that maintain their clinical efficacy without contributing to the development of diabetes mellitus and other proatherogenic effects.
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Skeletal muscle insulin resistance can develop secondary to pharmacological therapy, including glucocorticoids, anti-HIV therapy, and beta blockers.
“Insulin resistance in skeletal muscle also can develop secondary to pharmacological therapy, for example, glucocorticoids [44], anti-HIV therapy [45], and beta blockers [46].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [45]
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- [38]Callebaut C Yan Q Koster J GS-8374, a novel HIV protease inhibitor, does not alter peripheral glucose disposal in a healthy rodent model system 15th Conference on Retroviruses and Opportunistic Infections 2008 February 3–6 2008 Boston, Massachusetts This study illustrates the utility of in-vitro screening of candidate protease inhibitors for their ability to influence glucose uptake prior to large and costly clinical trials.
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- Authors
- Hruz, P. W.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Hruz, Paul W
- ORCID
- Hruz, Paul W
- Venue
- Current Opinion in HIV and AIDS
- Published
- 2008-11
- Volume
- 3
- Issue
- 6
- Pages
- 660-665
- ISSN
- 1746-630X (ISSN-L)
- PMC
- PMC2680222
- OpenAlex
- W2041972566
- Cited by
- 49
- References
- 56
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 3 · 2023: 4 · 2021: 6 · 2020: 7 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 4 · 2014: 1 · 2013: 2
- FWCI
- 2.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in HIV and AIDS (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK064572)
- Topics
- Health Sciences › Medicine › Emergency Medicine › HIV-related health complications and treatments
- Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- HIV protease inhibitors, insulin resistance, glucose transporter 4, oxidative stress, proteasome inhibition, adipokines, SOCS1, diabetes mellitus, cardiovascular risk, glucose homeostasis, pharmacokinetics
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