Steven Grinspoon

Harvard University, Cambridge, Massachusetts, United States

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Publications (260)1952.19 Total impact

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    ABSTRACT: Objective: Circulating oxidized low-density lipoprotein (oxLDL) levels are elevated in HIV-infected patients and have been associated with subclinical atherosclerosis. Statins have been shown to reduce plaque on coronary computed tomography angiography (cCTA) in HIV-infected individuals. Thus, we investigated the effect of statins on serum oxLDL levels and the relationship between changes in oxLDL and coronary atherosclerosis on cCTA in patients with HIV. Design: We previously conducted a 12-month randomized, placebo-controlled trial with atorvastatin in 40 HIV-infected patients on stable antiretroviral therapy with subclinical coronary atherosclerosis and low-density lipoprotein (LDL)-cholesterol less than 130 mg/dl. Methods: In the current analysis, patients underwent cCTA and measurements of serum oxLDL, sCD14, sCD163, lipoprotein phospholipase-A2, and fasting lipids including direct LDL at baseline and end of the study. Results: Nineteen patients were randomized to atorvastatin and 21 patients to placebo. Serum oxLDL decreased -22.7% (95% CI -28.7 to -16.7) in the atorvastatin group and increased 7.5% (95% CI -3.3 to 18.4) in the placebo group (P < 0.0001). Change in oxLDL significantly correlated with changes in noncalcified plaque volume, total plaque volume, positively remodeled plaque, and low attenuation plaque. The association between changes in oxLDL and noncalcified plaque volume was independent of the baseline 10-year Framingham risk, direct LDL, CD4 cell count, and viral load. Conclusion: Statins lower oxLDL levels in HIV-infected patients, and reductions in oxLDL are related to improvements in coronary atherosclerosis, independent of traditional cardiovascular risk factors. Reductions in oxLDL may be one mechanism through which statins exert beneficial effects on reducing atherosclerosis in HIV-infected individuals.
    AIDS (London, England) 11/2015; DOI:10.1097/QAD.0000000000000946 · 5.55 Impact Factor

  • AIDS 10/2015; DOI:10.1097/QAD.0000000000000902 · 5.55 Impact Factor
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    ABSTRACT: Little is known about renin-angiotensin-aldosterone system (RAAS) activation in relationship to visceral adipose tissue (VAT) accumulation in HIV-infected patients, a population at significant risk for insulin resistance and other metabolic disease. Twenty HIV and ten non-HIV-infected subjects consumed a standardized low sodium or liberal sodium diet, to stimulate or suppress the RAAS, respectively. RAAS parameters were evaluated in response to each diet and a graded angiotensin II infusion. Further analyses were performed after groups were substratified by median VAT measured by MRI. Aldosterone concentrations during the low sodium diet were higher in HIV than non-HIV-infected subjects(13.8 [9.7, 30.9] vs. 9.2 [7.6, 13.6]ng/dL,P=0.03) and increased across groups stratified by VAT(8.5 [7.1, 12.8], 9.2 [8.1, 21.5], 11.4 [9.4, 13.8], 27.2 [13.0, 36.9] ng/dL in non-HIV-infected without increased VAT, non-HIV-infected with increased VAT, HIV-infected without increased VAT, HIV-infected with increased VAT, respectively, overall trend P=0.02). Under this condition, plasma renin activity(3.50 [2.58, 4.65] vs. 1.45 [0.58, 2.33]ng/ml/hr, P=0.002) was higher among the HIV-infected subjects with vs. without increased VAT. Differences in the suppressibility of PRA by graded angiotensin infusion were seen stratifying by VAT among the HIV-infected group(P < 0.02 at each dose). In addition, aldosterone(P=0.007) was an independent predictor of insulin resistance in multivariate modeling, controlling for VAT and adiponectin. These data suggest excess RAAS activation in relationship to visceral adiposity in HIV-infected patients that may independently contribute to insulin resistance. Mineralocorticoid blockade may have therapeutic potential to reduce metabolic complications in HIV-infected patients with increased visceral adiposity.
    The Journal of Clinical Endocrinology and Metabolism 06/2015; 100(8):jc20151461. DOI:10.1210/jc.2015-1461 · 6.21 Impact Factor
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    ABSTRACT: HIV-infected patients have a high risk of myocardial infarction. We aimed to assess the ability of statin treatment to reduce arterial inflammation and achieve regression of coronary atherosclerosis in this population.
    The Lancet HIV 02/2015; 2(2):e52-e63. DOI:10.1016/S2352-3018(14)00032-0
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    ABSTRACT: Some intestinal microbiota-generated metabolites of phosphatidylcholine are recognized to be proatherogenic. As the HIV population is vulnerable to cardiovascular disease and can develop intestinal dysbiosis associated with systemic inflammation, we investigated the novel relationship between microbiota-derived metabolites of phosphatidylcholine and coronary atherosclerosis in HIV. One hundred and fifty-five HIV-infected and 67 non-HIV-infected individuals without known history of cardiovascular disease were previously recruited to assess coronary plaque by computed tomography angiography. In the current study, we evaluate whether serum choline, trimethylamine (TMA), or trimethylamine-N-oxide (TMAO) levels are associated with plaque features. Young, asymptomatic HIV-infected patients (age 47 ± 7 years) demonstrated significantly higher prevalence of plaque (53 vs. 35%, P = 0.01) and number of total plaque segments (1.8 ± 2.5 vs. 1.2 ± 2.2, P = 0.03) when compared with well matched noninfected individuals with similar comorbidities. TMA was significantly associated with calcium score (r = 0.22, P = 0.006), number of total (r = 0.20, P = 0.02) and calcified (r = 0.18, P = 0.03) plaque segments, and calcium plaque volume (r = 0.19, P = 0.02) and mass (r = 0.22, P = 0.009) in the HIV cohort only. In multivariate modeling among HIV-infected patients, TMA remained significantly associated with calcium score (P = 0.008), number of total (P = 0.005) and calcified (P = 0.02) plaque segments, and calcium plaque volume (P = 0.01) and mass (P = 0.007), independent of Framingham risk score. In contrast, there was no association of TMAO to coronary plaque features in either cohort. A link between TMA and atherosclerosis has not previously been established. The current study suggests that TMA may be a nontraditional risk factor related to the number of plaque segments and severity of calcified plaque burden in HIV.
    AIDS (London, England) 01/2015; 29(4). DOI:10.1097/QAD.0000000000000565 · 5.55 Impact Factor
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    Ahmed Tawakol · Steven K Grinspoon ·
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    ABSTRACT: HIV disease, left inadequately treated, leads to an inexorable decline in immune function resulting in AIDS and ultimately in death from opportunistic infections. However, advances in treatment of HIV have resulted in a dramatic reduction in AIDS-related mortality.1 With the widespread use of highly active antiretroviral therapy (HAART), HIV infection has been transformed to a chronic disease associated with long-term viral suppression but at the cost of an increase in atherothrombotic diseases.2,3 Hence currently there is substantial interest in developing a better understanding of the mechanisms underlying the increased risk of atherothrombosis in HIV disease.While HIV infection is characterized by a decline of peripheral blood CD4+ T cells, a paradoxical chronic immune activation of T cells and monocytes is routinely seen in virally suppressed HIV disease.4-6 Multiple studies in HIV-infected individuals show that this persistently heightened state of immune activation likely contrib ...
    Journal of Nuclear Cardiology 12/2014; 22(2). DOI:10.1007/s12350-014-0044-9 · 2.94 Impact Factor
  • Takara L. Stanley · Steven K. Grinspoon ·
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    ABSTRACT: Increased visceral adipose tissue (VAT) is associated with reductions in endogenous GH secretion, possibly as a result of hyperinsulinemia, increased circulating free fatty acid, increased somatostatin tone, and reduced ghrelin. Reduced GH may, in turn, further exacerbate visceral fat accumulation because of decreased hormone sensitive lipolysis in this depot. Data from multiple populations demonstrate that both reduced GH and increased VAT appear to contribute independently to dyslipidemia, increased systemic inflammation, and increased cardiovascular risk. The reductions in GH in states of visceral adiposity are characterized by reduced basal and pulsatile GH secretion with intact pulse frequency. Treatment with GH releasing hormone (GHRH) provides a means to reverse these abnormalities, increasing endogenous basal and pulsatile GH secretion without altering pulse frequency. This review describes data from HIV-infected individuals and individuals with general obesity showing that treatment with GHRH significantly reduces visceral fat, ameliorates dyslipidemia, and reduces markers of cardiovascular risk. Further research is needed regarding long term efficacy and safety of this treatment modality.
    Growth Hormone & IGF Research 12/2014; 25(2). DOI:10.1016/j.ghir.2014.12.005 · 1.41 Impact Factor
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    Sujit Suchindran · Susan Regan · James B Meigs · Steven K Grinspoon · Virginia A Triant ·
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    ABSTRACT: Human immunodeficiency virus (HIV) infection is associated with increased risk of myocardial infarction (MI). The use of aspirin for primary and secondary MI prevention in HIV infection has not been extensively studied. We performed a cross-sectional study of 4037 patients infected with HIV and 36 338 demographics-matched control patients in the Partners HealthCare System HIV cohort. We developed an algorithm to ascertain rates of nonepisodic acetylsalicylic acid (ASA) use using medication and electronic health record free text data. We assessed rates of ASA use among HIV-infected and HIV-uninfected (negative) patients with and without coronary heart disease (CHD). Rates of ASA use were lower among HIV-infected compared with HIV-uninfected patients (12.4% vs 15.3%, P < .001), with a relatively greater difference among patients with ≥2 CHD risk factors (22.1% vs 42.4%, P < .001). This finding was present among men and among patients in the 30-39 and 40-49 age groups. Among patients with prevalent CHD using ASA for secondary prevention, rates of ASA use were also lower among HIV-infected patients compared with HIV-uninfected patients (51.6% vs 65.4%, P < .001). Rates of ASA use were lower among HIV-infected patients compared with controls, with a greater relative difference among those with elevated CHD risk and those with known CHD. Further studies are needed to investigate the optimal strategies for ASA use among patients infected with HIV.
    12/2014; 1(3):ofu076. DOI:10.1093/ofid/ofu076
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    ABSTRACT: Individuals infected with human immunodeficiency virus (HIV) have decreased high-density lipoprotein (HDL)-cholesterol and increased cardiovascular disease (CVD). Reverse cholesterol transport from macrophages may be inhibited by HIV and contribute to increased CVD. Human studies have not investigated longitudinal effects of HIV and antiretroviral therapy (ART) on cholesterol efflux. Subjects with acute HIV infection were randomized to ART or not. Cholesterol efflux capacity was determined ex vivo after exposure of murine macrophages to apolipoprotein B-depleted patient sera obtained at baseline and after 12 weeks. After 12 weeks, HIV RNA decreased most in subjects randomized to ART. Available data on cholesterol demonstrated that efflux capacity from Abca1(+/+) macrophages was increased most by sera obtained from ART-treated subjects (20.5% ± 5.0% to 24.3 % ± 6.9%, baseline to 12 weeks, P = .007; ART group [n = 6] vs 18.0 % ± 3.9% to 19.1 % ± 2.9%, baseline to 12 weeks, P = .30; untreated group [n = 6] [P = .04 ART vs untreated group]). Change in HIV RNA was negatively associated with change in Abca1(+/+) macrophage cholesterol efflux (r = - 0.62, P = .03), and this finding remained significant (P = .03) after controlling for changes in HDL-cholesterol, CD4(+) cells, and markers of monocyte or macrophage activation. In subjects acutely infected with HIV, ATP-binding cassette transporter A1-mediated cholesterol efflux was stimulated to a greater degree over time by apolipoprotein B-depleted serum from subjects randomized to ART. The improvement in cholesterol efflux capacity is independently related to reduction in viral load.
    12/2014; 1(3):ofu108. DOI:10.1093/ofid/ofu108
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    ABSTRACT: Background: Heightened immune activation among human immunodeficiency virus (HIV)-infected persons may contribute to atherosclerosis. We assessed associations of serologic markers of monocyte activation, soluble CD163 (sCD163) and soluble CD14 (sCD14), and monocyte chemoattractant protein 1 (CCL2) with subclinical atherosclerosis among men with and those without HIV infection in the Multicenter AIDS Cohort Study. Methods: We performed noncontrast computed tomography on 906 men (566 HIV-infected men and 340 HIV-uninfected men), 709 of whom also underwent coronary computed tomographic angiography. Associations between each biomarker and the prevalence of coronary plaque, the prevalence of stenosis of ≥50%, and the extent of plaque were assessed by logistic and linear regression, adjusting for age, race, HIV serostatus, and cardiovascular risk factors. Results: Levels of all biomarkers were higher among HIV-infected men, of whom 81% had undetectable HIV RNA, and were associated with lower CD4(+) T-cell counts. In the entire population and among HIV-infected men, higher biomarker levels were associated with a greater prevalence of coronary artery stenosis of ≥50%. Higher sCD163 levels were also associated with greater prevalences of coronary artery calcium, mixed plaque, and calcified plaque; higher CCL2 levels were associated with a greater extent of noncalcified plaque. Conclusions: sCD163, sCD14, and CCL2 levels were elevated in treated HIV-infected men and associated with atherosclerosis. Monocyte activation may increase the risk for cardiovascular disease in individuals with HIV infection.
    The Journal of Infectious Diseases 10/2014; 211(8). DOI:10.1093/infdis/jiu594 · 6.00 Impact Factor
  • Markella V Zanni · Judith Schouten · Steven K Grinspoon · Peter Reiss ·
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    ABSTRACT: The lives of individuals infected with HIV who have access to combination antiretroviral therapy (cART) are substantially prolonged, which increases the risk of developing non-AIDS comorbidities, including coronary heart disease (CHD). In Europe and the USA, individuals with HIV infection have a ∼1.5-fold increased risk of myocardial infarction relative to uninfected individuals. In Africa, the relative risk of myocardial infarction is unknown, but broadened access to life-extending cART suggests that rates of CHD will rise in this and other resource-constrained regions. Atherogenesis in HIV is affected by complex interactions between traditional and immune risk factors. cART has varied, regimen-specific effects on metabolic risk factors. Overall, cART seems to lessen proatherogenic immune activation, but does not eliminate it even in patients in whom viraemia is suppressed. Current strategies to decrease the risk of CHD in individuals infected with HIV include early initiation of cART regimens with the fewest metabolic adverse effects, and careful management of traditional CHD risk factors throughout treatment. Future strategies to prevent CHD in patients with HIV infection might involve the use of HIV-tailored CHD risk-prediction paradigms and the administration of therapies alongside cART that will further decrease proatherogenic HIV-specific immune activation.
    Nature Reviews Cardiology 10/2014; 11(12). DOI:10.1038/nrcardio.2014.167 · 9.18 Impact Factor
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    ABSTRACT: Objective: To compare rates of intracerebral hemorrhage (ICH) in HIV-infected and uninfected individuals in a large clinical care cohort and to assess risk factors associated with ICH. Methods: We identified incident ICH in HIV-infected and uninfected control cohorts from the Partners Health Care system using ICD-9-CM codes. We constructed Cox proportional hazards models to estimate adjusted hazard ratios for HIV infection and other predictors of ICH. Results: The incidence rate of ICH was 2.29 per 1,000 person-years in HIV-infected individuals compared with 1.23 per 1,000 person-years in uninfected individuals, with an unadjusted incidence rate ratio of 1.85 (95% confidence interval 1.37-2.47, p < 0.001). In a multivariable model, HIV infection was independently associated with a higher hazard of ICH, although its effect diminished with increasing age. Female sex was associated with a lower hazard of ICH in the uninfected cohort but not in the HIV cohort. CD4 count <200 × 10(6) cells/L and anticoagulant use were predictive of ICH. Conclusions: HIV infection conferred an increased adjusted hazard of ICH, which was more pronounced in young patients and in women.
    Neurology 10/2014; 83(19). DOI:10.1212/WNL.0000000000000958 · 8.29 Impact Factor
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    ABSTRACT: Background: The 2013 American College of Cardiology/American Heart Association (ACC/AHA) cholesterol guidelines are being applied to HIV-infected patients but have not been validated in this at-risk population, which is known to have a high prevalence of subclinical high-risk morphology (HRM) coronary atherosclerotic plaque. Objective: To compare recommendations for statins among HIV-infected subjects with/without HRM coronary plaque according to 2013 ACC/AHA versus 2004 Adult Treatment Panel III guidelines. Methods/design: Data from 108 HIV-infected subjects without known cardiovascular disease (CVD) or lipid-lowering treatment who underwent contrast-enhanced computed tomography angiography were analyzed. Recommendations for statin therapy according to 2013 versus 2004 guidelines were assessed among those with/without HRM coronary plaque. Results: Among all subjects, 10-year atherosclerotic cardiovascular disease (ASCVD) risk score was 3.3% (1.6, 6.6), yet 36% of subjects had HRM coronary plaque. Among those with HRM coronary plaque, statins would be recommended for 26% by 2013 guidelines versus 10% by 2004 guidelines (P=0.04). Conversely, among those without HRM coronary plaque, statins would be recommended for 19% by 2013 guidelines versus 7% by 2004 guidelines (P=0.005). In multivariate modeling, while 10-year ASCVD risk score related to HRM coronary plaque burden (P=0.02), so too did other factors not incorporated into 2013 guidelines. Conclusion: The 2013 ACC/AHA cholesterol guidelines recommend statin therapy for a higher percentage of subjects with and without HRM coronary plaque relative to 2004 guidelines. However, even by 2013 guidelines, statin therapy would not be recommended for the majority (74%) of HIV-infected subjects with subclinical HRM coronary plaque. Outcome studies are needed to determine the utility of new statin recommendations and the contribution of HRM coronary plaque to CVD events among HIVinfected subjects.
    AIDS (London, England) 09/2014; 28(14):2061-2070. DOI:10.1097/QAD.0000000000000360 · 5.55 Impact Factor
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    ABSTRACT: Telomere length (TL) and immune activation markers were measured in a cohort of HIV-infected (n=102) and age-matched non-HIV-infected (n=41) men. TL was significantly shorter in HIV-infected compared to non-HIV-infected subjects (P = 0.04). Univariate analysis revealed a strong inverse relationship of TL to sCD163, and thus, monocyte/macrophage activation, among the HIV group (ρ = -0.30, P = 0.003). In multivariate modeling among the whole group, HIV positive serostatus (P = 0.06) and sCD163 (P = 0.05) were independent predictors of TL controlling for age and smoking status. Our data demonstrate that increased immune activation relates to shorter TL in HIV.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 09/2014; 67(4). DOI:10.1097/QAI.0000000000000329 · 4.56 Impact Factor
  • Steven K Grinspoon ·
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    ABSTRACT: A new paradigm for atherogenesis in HIV infection is emerging, in which viral replication and microbial translocation result in ongoing T-cell and monocyte activation, with persistent inflammation leading to the development of atypical, high-risk morphology plaques. These plaques, characterized by low attenuation and positive remodeling, can be found even among HIV-infected patients who are at low risk for cardiovascular disease based on traditional risk factors. Prevention of cardiovascular events in HIV infection requires modulation of traditional risk factors and is also likely to require effective antiinflammatory treatment strategies. Statins, which are traditionally used to treat dyslipidemia, have also been shown to exert antiinflammatory effects associated with clinical benefit and may be useful to treat and prevent cardiovascular disease in HIV-infected patients. However, large-scale studies of statins in the context of HIV infection must be conducted. This article summarizes a presentation by Steven K. Grinspoon, MD, at the IAS-USA continuing education program held in Chicago, Illinois, in May 2014.
    Topics in antiviral medicine 09/2014; 22(4):676-679.
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    ABSTRACT: Background. Human immunodeficiency virus (HIV)-1 elite controllers (ECs) represent an ideal population to study the effects of HIV persistence on chronic inflammation in the absence of antiretroviral therapy (ART). Methods. Twenty inflammatory markers measured in cohorts of ECs, HIV suppressed noncontrollers, and HIV-uninfected controls were compared using rank-based tests and partial least squares discriminant analysis (PLSDA). Spearman correlations were determined among the inflammatory markers, residual viremia by the single-copy assay, and CD4[superscript +] T cell slope. Results. Significant differences were seen between cohorts in 15 of the soluble inflammatory markers. Human immunodeficiency virus-1 ECs were found to have the highest levels for all of the markers with the exception of RANTES. In particular, median levels of 7 inflammatory markers (soluble CD14 [sCD14], interferon [IFN]-γ, IFN-γ-inducible protein [IP]-10, interleukin [IL]-4, IL-10, sCD40L, and granulocyte-macrophage colony-stimulating factor) were twice as high in the HIV-1 ECs compared with either of the HIV-suppressed or uninfected groups. Multivariate PLSDA analysis of inflammatory markers improved differentiation between the patient cohorts, discerning gender differences in inflammatory profile amongst individuals on suppressive ART. Soluble markers of inflammation in ECs were not associated with either levels of residual HIV-1 viremia or CD4[superscript +] T cell decline. Conclusions. Despite maintaining relatively low levels of viremia, HIV-1 ECs had elevated levels of a set of key inflammatory markers. Additional studies are needed to determine whether ECs may benefit from ART and to further evaluate the observed gender differences.
    08/2014; 2(1):ofu117-ofu117. DOI:10.1093/ofid/ofu117
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    ABSTRACT: Objective Few studies have investigated irisin and FGF21 to elucidate the role of these hormones to regulate “beiging” in HIV-infected patients.Design50 HIV-infected subjects with the metabolic syndrome were previously recruited and randomized to receive lifestyle modification(LSM) and/or metformin over 12 months. In the current study, we assessed FGF21 and irisin at baseline and after intervention. In addition, we assessed circulating FGF21 and irisin in relationship to brown adipose tissue(BAT) gene expression in dorsocervical subcutaneous fat biopsies from 13 HIV-infected subjects.ResultsAt baseline, prior to intervention, HIV-infected subjects demonstrated increased log FGF21 (2.13±0.06 vs. 1.98±0.05 pg/mL, P=0.05) and log irisin (0.33±0.02 vs. 0.17±0.04 μg/mL, P=0.003) compared to healthy controls well-matched based on waist circumference. After 12 months, HIV-infected subjects randomized to LSM demonstrated a relative reduction in FGF21 compared to those not randomized to LSM (-10[-35,22]) vs. 40[0,94] %change, P=0.01). Changes in FGF21 were inversely associated with improved parameters of energy homeostasis, including increased REE (ρ=-0.34, P=0.046) and max VO2 (ρ=-0.38, P=0.02), and reduced RQ (ρ=0.40, P=0.02) among all HIV-infected subjects. Increased UCP-1 (r=0.75, P=0.003), DIO2 (r=0.58, P=0.04), and CideA(r=0.73, P=0.01) gene expression in dorsocervical fat was significantly associated with FGF21 in HIV-infected subjects.ConclusionHIV-infected subjects with metabolic complications demonstrate increases in FGF21 in relationship to BAT gene expression. Relative reductions in FGF21 in those receiving long-term LSM relate to overall improvements in energy expenditure parameters. In contrast, irisin levels are elevated in HIV-infected subjects, but are not influenced by LSM nor associated with BAT gene expression.This article is protected by copyright. All rights reserved.
    Clinical Endocrinology 08/2014; 82(5). DOI:10.1111/cen.12582 · 3.46 Impact Factor
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    ABSTRACT: Among patients infected with human immunodeficiency virus (HIV), visceral adiposity is associated with metabolic dysregulation and ectopic fat accumulation. Tesamorelin, a growth hormone-releasing hormone analog, specifically targets visceral fat reduction but its effects on liver fat are unknown.
    JAMA The Journal of the American Medical Association 07/2014; 312(4):380-9. DOI:10.1001/jama.2014.8334 · 35.29 Impact Factor
  • Steven Grinspoon ·

    AIDS (London, England) 07/2014; 28(11):1679-1681. DOI:10.1097/QAD.0000000000000117 · 5.55 Impact Factor
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    ABSTRACT: miRNAs are important regulators of biological processes in many tissues, including the differentiation and function of brown and white adipocytes. The endoribonuclease dicer is a major component of the miRNA-processing pathway, and in adipose tissue, levels of dicer have been shown to decrease with age, increase with caloric restriction, and influence stress resistance. Here, we demonstrated that mice with a fat-specific KO of dicer develop a form of lipodystrophy that is characterized by loss of intra-abdominal and subcutaneous white fat, severe insulin resistance, and enlargement and "whitening" of interscapular brown fat. Additionally, KO of dicer in cultured brown preadipocytes promoted a white adipocyte-like phenotype and reduced expression of several miRNAs. Brown preadipocyte whitening was partially reversed by expression of miR-365, a miRNA known to promote brown fat differentiation; however, introduction of other miRNAs, including miR-346 and miR-362, also contributed to reversal of the loss of the dicer phenotype. Interestingly, fat samples from patients with HIV-related lipodystrophy exhibited a substantial downregulation of dicer mRNA expression. Together, these findings indicate the importance of miRNA processing in white and brown adipose tissue determination and provide a potential link between this process and HIV-related lipodystrophy.
    Journal of Clinical Investigation 07/2014; 124(8). DOI:10.1172/JCI73468 · 13.22 Impact Factor

Publication Stats

13k Citations
1,952.19 Total Impact Points


  • 1999-2015
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1994-2014
    • Massachusetts General Hospital
      • • Department of Radiology
      • • Neuroendocrine Unit
      • • Department of Medicine
      Boston, Massachusetts, United States
  • 1970-2014
    • Harvard Medical School
      • • Department of Medicine
      • • Department of Radiology
      Boston, Massachusetts, United States
  • 2005-2011
    • Mass General Hospital
      Boston, Massachusetts, United States
    • U.S. Food and Drug Administration
      Washington, Washington, D.C., United States
  • 2007
    • McGill University Health Centre
      Montréal, Quebec, Canada
  • 2004
    • Massachusetts Institute of Technology
      Cambridge, Massachusetts, United States
  • 2003
    • University of California, San Francisco
      • Division of Hospital Medicine
      San Francisco, California, United States
  • 2002-2003
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States
  • 1992-1994
    • Columbia University
      • Department of Medicine
      New York, New York, United States