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PubMed2003

The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.

The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes have been debated extensively. The concept that a feedback loop governs the interaction of the insulin-sensitive tissues and the beta cell as well as the elucidation of the hyperbolic relationship between insulin sensitivity and insulin secretion explains why insulin-resistant subjects exhibit markedly increased insulin responses while those who are insulin-sensitive have low responses. Consideration of this hyperbolic relationship has helped identify the critical role of beta-cell dysfunction in the development of Type 2 diabetes and the demonstration of reduced beta-cell function in high risk subjects. Furthermore, assessments in a number of ethnic groups emphasise that beta-cell function is a major determinant of oral glucose tolerance in subjects with normal and reduced glucose tolerance and that in all populations the progression from normal to impaired glucose tolerance and subsequently to Type 2 diabetes is associated with declining insulin sensitivity and beta-cell function. The genetic and molecular basis for these reductions in insulin sensitivity and beta-cell function are not fully understood but it does seem that body-fat distribution and especially intra-abdominal fat are major determinants of insulin resistance while reductions in beta-cell mass contribute to beta-cell dysfunction. Based on our greater understanding of the relative roles of insulin resistance and beta-cell dysfunction in Type 2 diabetes, we can anticipate advances in the identification of genes contributing to the development of the disease as well as approaches to the treatment and prevention of Type 2 diabetes.

Adipose Tissue↗

PubMed1996

Phenotypic characterization of the Trp64Arg polymorphism in the beta 3-adrenergic receptor gene in normal weight and obese subjects.

The beta 3-adrenergic receptor, located mainly in fat cells of visceral adipose tissue, is involved in the regulation of lipolysis and thermogenesis. Recently, a mutation in the corresponding gene resulting in the replacement of tryptophan by arginine in position 64 (Trp64Arg) has been demonstrated, which associated with obesity and metabolic complications of obesity. We have investigated whether this polymorphism is associated with changes in beta 3-adrenergic receptor function or clinical characteristics in 40 non-obese and 43 obese non-diabetic subjects who underwent elective abdominal surgery. The beta-adrenergic receptor gene polymorphism was examined by restriction-enzyme cleavage conformation. Beta 3-adrenergic receptor function was investigated by measuring lipolysis in isolated visceral white fat cells incubated with noradrenaline (natural ligand) or (CGP) 12,177 (selective beta 3-agonist). No homozygotes for the mutation were found. The allelic frequency of Trp64Arg was similar in obese and non-obese subjects (9.4 and 12.5%, respectively). In obese and non-obese subjects there was no change in body mass index, body fat distribution, fat cell size, fasting circulating levels of insulin, glucose or lipids, blood pressure or adipocyte lipolysis induced by noradrenaline or CGP 12,177 when Trp64Arg heterozygotes were compared with Trp64A homozygotes. Our results suggest that the Trp64Arg mutation in its heterozygous form is not a major determinant of beta 3-adrenergic receptor function (when assessed by lipolysis in white adipose tissue) or of the pathophysiology of obesity.

Adipocytes↗

PubMed2005

[Role of body weight for the prevention of coronary heart disease].

The prevalence of obesity has increased considerably in recent years; only one third of our population displays a desirable, healthy weight. Persons with increased body fat mass are in a constant pro-inflammatory and pro-thrombotic condition; in addition they are often insulin-resistant und show cardiovascular risk factors. Therefore, obesity induces the development of atherosclerosis as an independent risk factor as well as a promoter for other risk factors. In addition, congestive heart failure is more frequent in obese subjects. By reducing body weight with a decrease of predominantly visceral fat all risk factors are improved as well as endothelial function. Effects on coronary atherosclerosis and congestive heart disease are until now insufficiently investigated.

Body Fat Distribution↗

PubMed2006

Prevalence of lipodystrophy in HIV-infected children: a cross-sectional study.

OBJECTIVE: The aim of this study was to assess the changes in body fat distribution and lipid abnormalities in a population of HIV-infected children and adolescents followed in one single centre who had been exposed, or not, to antiretroviral therapy (ART). MATERIALS AND METHODS: Patients aged between 3 and 19 years were evaluated in a cross-sectional study carried out between October and December 2002. Fat redistribution was evaluated independently by the physician and the patient. Fasting blood lipid profile, glucose, insulin and C peptide were measured. Among the 88 patients evaluated, 74 were taking ART. RESULTS: Fat redistribution was present in 20 patients, metabolic alterations alone were found in 22 children and 46 children had neither physical nor metabolic abnormalities. Patients with fat redistribution were found to have been on ART for a significantly longer period of time, with 42% of the children showing fat redistribution having been treated with antiretroviral agents for more than 5 years. These children had also been exposed to a higher number of antiretroviral agents. In contrast, metabolic alterations in the absence of fat redistribution were not related to the duration of ART nor to the number of drugs received. Treatment with stavudine or protease inhibitors was significantly associated with the presence of physical changes. CONCLUSION: Regular assessment of fat redistribution and metabolic markers should be carried out in children treated with antiretroviral agents and taken into account when adapting therapy during the long-term follow up of these children.

Adolescent↗

PubMed1998

Transmission disequilibrium and sequence variants at the leptin receptor gene in extremely obese German children and adolescents.

Genetic determinants of the degree of obesity and body fat distribution have been demonstrated by family studies. The heritability has been estimated to be in the range 0.2-0.7. Mutation leading to obesity in humans has been described for only two genes, one of them the leptin gene. The leptin gene codes for a cytokine secreted by fat cells that binds to the leptin receptor (Lep-R), which exerts some of its biological functions by expression in the brain. Hence, the Lep-R gene appears to be a promising candidate for the determination of obesity in humans. We isolated genomic DNA clones from the Lep-R gene region and identified a new polymorphic microsatellite marker (OBR-CA) within 80 kb of the translation start of Lep-R. We genotyped this and a second, intragenic microsatellite marker (D1S2852) in 130 nuclear families consisting of extremely obese children and adolescents and both parents. Using the most frequent parental allele of both markers, our analysis revealed a significant transmission disequilibrium for the 266-bp allele of D1S2852 (corrected P-value=0.042). No significant result was obtained with the most frequent allele of OBR-CA (corrected P-value=1.0). However, two rare alleles showed transmission disequilibrium and were subsequently used for constructing a haplotype with the 266-bp allele. This haplotype had a transmission rate of 80% (nominal P-value=0.02). In order to identify the underlying mutation, we sequenced all coding exons of Lep-R and the partially overlapping gene encoding the obese receptor gene-related protein (ob-rgrp) in individuals carrying this haplotype. We found one new mutation (Ser675Thr) in the Lep-R gene in one proband and several other mutations known to be not associated with obesity in other study groups. As this new mutation cannot explain our positive linkage result, the transmission disequilibrium of the 266-bp allele and the high transmission rate of the identified haplotype point towards a mutation in close proximity to marker D1S2852.

Adolescent↗

PubMed2006

Seasonal thermogenesis and body mass regulation in plateau pikas (Ochotona curzoniae).

Changes in photoperiod, ambient temperature and food availability trigger seasonal acclimatization in physiology and behavior of many animals. In the present study, seasonal adjustments in body mass and in several physiological, hormonal, and biochemical markers were examined in wild-captured plateau pikas (Ochotona curzoniae) from the Qinghai-Tibetan plateau. Our results showed that plateau pikas maintained a relatively constant body mass throughout the year and showed no seasonal changes in body fat mass and circulating levels of serum leptin. However, nonshivering thermogenesis, cytochrome c oxidase activity, and mitochondrial uncoupling protein 1 (UCP1) contents in brown adipose tissues were significantly enhanced in winter. Further, serum leptin levels were positively correlated with body mass and body fat mass while negatively correlated with UCP1 contents. Together, these data suggest that plateau pikas mainly depend on increasing thermogenic capacities, rather than decreasing body mass, to cope with cold, and leptin may play a potential role in their thermogenesis and body mass regulation.

Acclimatization↗

PubMed2006

[Antipsychotic drug-induced changes in metabolism].

Antipsychotic medications are a mainstay in the treatment of schizophrenia and are widely used in other psychiatric conditions. New generation antipsychotic agents (NGAs) are increasingly replacing first generation antipsychotic agents (FGAs), mainly due to a decreased risk for extrapyramidal symptoms, better overall tolerability, as well as some efficacy advantages. However, some of these NGAs are associated with adverse metabolic effects such as substantial weight gain, the induction of insulin resistance and lipid disorders. Among these substances, clozapine and olanzapine induce the most significant weight gain, olanzapine mainly by increasing body fat and both of these antipsychotics have been associated with disturbances in glucose metabolism. Diabetes mellitus induced by treatment with some NGAs occurred in many cases within days to weeks after initiation of SGA therapy, in some cases hyperglycemia promptly resolved after discontinuation of the medication and several reports have documented recurrent hyperglycemia after a rechallenge with the same drug. One possible pathomechanism for hyperglycemia induced by these NGAs is the induction of insulin resistance via humoral and/or cellular pathways. Alternatively, NGA induced diabetes may occur because of weight gain or a change in body fat distribution with a shift to a predominantly visceral fat type or through a direct effect on insulin sensitive target tissues. In this article we like to review the metabolic side effects of NGA treatment, highlight recent advances in the pathogenesis of these metabolic complications and discuss potential treatments of these side effects.

Antipsychotic Agents↗

PubMed2006

Concurrent and separate effects of body mass index and waist-to-hip ratio on 24-year mortality in the Population Study of Women in Gothenburg: evidence of age-dependency.

Obesity is generally assumed to be an important risk factor for death and morbidity. However, the association between excess body weight and all-cause mortality among younger and older women and the impact of body mass index (BMI) and waist-to-hip ratio (WHR) concurrently is not fully understood. In 1968-1969 we initiated a prospective study comprising a population sample of 1,462 women from Gothenburg, Sweden. During a 24 year period, until 1992-1993, 265 women had died. A multivariable Cox Proportional Hazards Regression model was used to estimate the relative risk of death in relation to BMI and WHR, with age and other covariates of age-specific interest as smoking, physical activity at work and leisure time and serum triglyceride concentration, at start of the study. BMI and WHR were analyzed as independent variables. Younger women (38 and 46 years at baseline) presented a statistically significant non-linear (U-shaped) relation between BMI and mortality. Among older women (50, 54 and 60 years at baseline), a significant negative linear relationship with decreasing mortality in relation to increasing BMI values was seen. For all women a higher WHR was related to an increased risk of death. The lowest risk of death among younger women corresponded to a low WHR and a BMI within the middle range. For older women the highest survival was observed for those with lowest WHR and highest BMI. Thus, in older women a high BMI seems not to be an increased risk as long as adiposity is not centrally located.

Age Factors↗

PubMed2006

Coronary heart disease in women: why the disproportionate risk?

Women with diabetes experience much greater relative risks of coronary heart disease (CHD) compared with the nondiabetic population than do men with diabetes. In type 2 diabetes, much of the greater elevation in risk in women is explained by a more adverse pattern of known CHD risk factors. In type 1 diabetes the picture is less clear, but current evidence suggests that a cardioprotective lipid profile is found in type 1 diabetic men, thus reducing the effect of diabetes on CHD, but that in women this is not the case. Also, in type 1 diabetic women there is some evidence of altered body fat distribution and a greater elevation in blood pressure. Whether these reflect a greater degree of insulin resistance in type 1 women, and what the origin of this might be, remains controversial. The practical consequence is that clinicians need to be aware that the usual cardioprotective effect of sex does not apply in diabetic women and that risk factor intervention is needed at an early age.

Artifacts↗

PubMed1991

Polycystic ovary syndrome and the androgen-insulin connection.

The association of hyperandrogenism, insulin resistance, and polycystic ovarian disease is well established. The accompanying hyperinsulinemia results in acanthosis nigricans, an epiphenomenon of this syndrome. The knowledge that states of insulin resistance of diverse causes are associated with ovarian hyperandrogenism makes the argument for insulin-driven ovarian androgen secretion compelling. However, equally compelling evidence suggests that hyperandrogenism may contribute to insulin resistance and hyperinsulinemia. The irreconcilable differences between these two hypotheses have resulted in an array of contradictory studies. In this article a unified concept of polycystic ovary syndrome and its androgen-insulin connection is proposed. The hypothesis incorporates the role of hyperinsulinemia in the androgen excess observed (and vice versa); the key to this connection is the androgen-dependent change in regional body fat distribution and its metabolic consequence. The pathophysiologic features of polycystic ovary syndrome, which has important clinical sequelae, deserve further consideration.

Androgens↗

PubMed1994

The effects of hormonal replacement therapy on insulin sensitivity in surgically postmenopausal cynomolgus monkeys (Macaca fascicularis).

OBJECTIVE: Our purpose was to evaluate the effect of hormone replacement therapy on insulin resistance in postmenopausal cynomolgus monkeys (Macaca fascicularis). STUDY DESIGN: We studied 37 surgically postmenopausal cynomolgus monkeys that were fed a moderately atherogenic diet for 12 weeks with either no treatment (control), conjugated equine estrogens, medroxyprogesterone acetate, combination conjugated equine estrogens and medroxyprogesterone acetate, or tamoxifen. Insulin sensitivity and glucose effectiveness were determined by the frequent-sampling intravenous tolerance test by means of the minimal model analysis. RESULTS: There were no differences in body weight, total plasma cholesterol, or body fat distribution between control and conjugated equine estrogens, medroxyprogesterone acetate, or combination treatment groups. However, compared with control animals (insulin sensitivity = 5.9 +2- 1.2 x 10(-4) min-1 microU-1 ml) or conjugated equine estrogens treatment (6.3 +/- 1.1 x 10(-4) min-1 microU-1 ml) insulin sensitivity was significantly decreased in animals treated with medroxyprogesterone acetate (2.9 +/- 0.4 x 10(-4) min-1 microU-1 ml, p < 0.001) or conjugated equine estrogens and medroxyprogesterone acetate (2.8 +/- 0.6 x 10(-4) min-1 microU-1 ml, p < 0.001). Although insulin sensitivity was shown to be decreased in the tamoxifen-treated animals (insulin sensitivity = 4.6 +/- 0.6 x 10(-4) min-1 microU -1 ml), the difference was not statistically significant compared with the control or conjugated equine estrogens-treated animals. No significant differences were seen for glucose effectiveness comparing control animals (glucose effectiveness = 0.043 +/- 0.006 min-1) to animals treated with medroxyprogesterone acetate (glucose effectiveness = 0.046 +/- 0.009 min-1), conjugated equine estrogens and medroxyprogesterone acetate (0.048 +/- 0.008 min-1) or tamoxifen (0.039 +/- 0.006 min-1). CONCLUSION: These results suggest that progestins alone or in combination with estrogens can induce insulin resistance in postmenopausal monkeys while having no effect on plasma lipid concentrations or glucose effectiveness.

Animals↗

PubMed1992

Beta-cell hypersecretion and not reduced hepatic insulin extraction is the main cause of hyperinsulinemia in obese nondiabetic subjects.

Obesity is characterized by peripheral hyperinsulinemia, for which either beta-cell hypersecretion, diminished hepatic insulin extraction, or both may be responsible. To clarify this issue, we investigated insulin secretion and hormone hepatic extraction in 18 nondiabetic obese patients (body mass index [BMI], 39 +/- 1.3 kg/m2) and 18 healthy, lean control subjects (BMI, 21.3 +/- 0.7 kg/m2). Body fat distribution was calculated by measuring the waist to hip ratio (WHR). A highly reduced tissue insulin sensitivity (2.4 +/- 0.5 v 9.5 +/- 1.5 10(4).min-1/[microU/mL], P > .0005) and glucose effectiveness, ie, glucose's ability to stimulate its own disappearance at basal insulin (16 +/- 2 v 30 +/- 3 10(3).min-1, P > .005), were found in the overweight subjects compared with the controls. The basal (76 +/- 14 v 37 +/- 4 pmol/L/min) and total (377,848 +/- 5,562 v 16,864 +/- 1,850 pmol/L) prehepatic insulin secretion and the basal (15 +/- 2 v 7 +/- 0.7 pmol/L/min) and total (8,286 +/- 2,009 v 2,840 +/- 210 pmol/L) posthepatic insulin delivery were significantly higher in the overweight subjects compared with the controls (P < .005), whereas the mean hepatic insulin extraction did not differ (77.8% +/- 2.6% v 79.5% +/- 2.6%). A significant inverse correlation was found between the hepatic insulin extraction and the WHR (r = .5, P > .04), signifying the importance of fat distribution in insulin metabolism. The obese patients were subdivided into two subgroups according to their glucose tolerance; eight patients exhibited a normal tolerance and the remaining 10 were intolerant.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

PubMed1994

Decreased testosterone and dehydroepiandrosterone sulfate concentrations are associated with increased insulin and glucose concentrations in nondiabetic men.

Although many studies indicate that increased androgenicity is associated with insulin resistance and hyperinsulinemia in both premenopausal and postmenopausal women, relatively few data are available on this relationship in men. We examined the association of sex hormone-binding globulin (SHBG), total and free testosterone, dehydroepiandrosterone sulfate (DHEA-SO4), and estradiol to glucose and insulin concentrations before and during an oral glucose tolerance test in 178 men from the San Antonio Heart Study, a population-based study of diabetes and cardiovascular disease. Total and free testosterone and DHEA-SO4 were significantly inversely associated with insulin concentrations. Free testosterone and DHEA-SO4 were also significantly inversely correlated with glucose concentrations. SHBG was weakly positively associated with glucose concentrations. Estradiol was not related to glucose or insulin concentrations. After adjustment for age, obesity, and body fat distribution, insulin concentrations remained significantly inversely correlated with free testosterone (r = -.23), total testosterone (r = -.21), and DHEA-SO4 (r = -.21; all P < .01). In conclusion, we observed that increased testosterone and DHEA-SO4 are associated with lower insulin concentrations in men. This is in striking contrast to women, where increased androgenicity is associated with insulin resistance and hyperinsulinemia.

Adult↗

PubMed1990

Obesity and osteoarthritis of the knee: evidence from the National Health and Nutrition Examination Survey (NHANES I).

The importance of systemic/metabolic factors in the association of obesity with radiographic knee osteoarthritis (OA) was examined for 3,905 adults aged 45 to 74 from the United States National Health and Nutrition Examination Survey, 1971 to 1975 (NHANES I). Obesity was associated with both bilateral and unilateral OA, but more strongly with bilateral OA. Obesity was also associated with both symptomatic and nonsymptomatic knee OA. Controlling for age, sex, serum cholesterol, serum uric acid, diabetes, body fat distribution, bone density, and blood pressure did not significantly reduce the association between obesity and knee OA. Findings from these data are not supportive of a metabolic link between obesity and knee OA.

Adult↗

PubMed1995

Interrelations between sex hormone-binding globulin (SHBG), plasma lipoproteins and cardiovascular risk.

The incidence of coronary artery disease is significantly higher in men than in women, at least until menopause. This gender difference could be explained by the action of sex steroids on the lipoprotein profile. In prepubertal children, high-density lipoprotein (HDL) cholesterol and triglyceride levels are similar between sexes, while adult men have generally lower HDL cholesterol and higher triglyceride levels than premenopausal adult women. Most cross-sectional studies have reported that sex hormone binding globulin (SHBG) and testosterone levels correlate positively with HDL cholesterol levels between sexes. Thus SHBG by modulating the balance in the biodisposal of testosterone and estradiol, might have a profound effect on the risk of cardiovascular disease. However, adjustment for body weight and body fat distribution weakens the association between SHBG, testosterone and HDL cholesterol. The negative correlation of fasting insulin with SHBG and HDL cholesterol levels in both sexes, and some evidence that insulin is an inhibitor of SHBG production in vitro, has suggested that hyperinsulinism might negatively regulate SHBG and HDL levels. It remains to be determined whether the inverse relationship between SHBG and insulin levels is coincidental or has a causal effect on the increase of atherosclerosis. Decreased SHBG has been shown to be predictive of the incidence of non-insulin-dependent diabetes mellitus in women but not in men, and of subsequent development of cardiovascular disease and overall mortality in postmenopausal women. SHBG is an index of androgenism in women and of insulin-resistance in both sexes, and might be useful in epidemiological studies of cardiovascular risk. However, in men, SHBG is not predictive of the occurrence of cardiovascular disease. Whether SHBG might have an intrinsic protective effect on the arterial wall through SHBG-receptors is still highly speculative.

Adult↗

PubMed1996

Predictors of myocardial lesions in men with minimal coronary atherosclerosis at autopsy. The Honolulu heart program.

Some cardiovascular risk factors are associated with clinical coronary heart disease but not with autopsy evidence of coronary atherosclerosis. To determine whether these risk factors might operate through mechanisms other than atherosclerosis, we examined associations between cardiovascular risk factors and subsequent intramural myocardial lesions assessed by protocol autopsy between 1965 and 1984 in 120 Japanese-American men from the Honolulu Heart Program who had minimal coronary atherosclerosis (American Heart Association (AHA) panel score < 3 on scale of 1 to 7). Age-adjusted prevalence of myocardial lesions was related to smoking status (P < 0.01), as well as amount, duration, and pack-years of smoking (P < 0.03). In a multiple logistic model, smoking (20 pack-years) was directly associated and fish intake (> or = 2 times/wk) was inversely associated with myocardial lesions independently of age, cholesterol, systolic blood pressure, body mass index, alcohol, diabetes, total calories, and animal protein intake (odds ratio (OR) = 1.5, 95% confidence intervals (CI) = 1.1 to 2.0 and OR = 0.35, 95% CI = 0.2 to 0.9, respectively). The protective effect of fish intake was most evident among men who did not have hypertension at baseline. Indices of obesity, body fat distribution, and physical activity and levels of triglyceride and alcohol intake were not associated with myocardial lesions. Thus, the adverse effects of smoking and the protective effects of fish consumption may extend to individuals relatively free of coronary atherosclerosis, possibly through hemostatic mechanisms or effects on small intramural arteries.

Aged↗

PubMed2006

Association between infant birth weight and maternal cardiovascular risk factors in the health, aging, and body composition study.

PURPOSE: Mothers who deliver a low-birth-weight (LBW) infant may themselves be at excess risk for cardiovascular disease. We investigated whether older women who bore LBW infants had higher blood pressure, lipid, glucose, insulin, interleukin 6 (IL-6), and C-reactive protein concentrations, and pulse wave velocity compared to women with normal-weight births. METHODS: Participants were 446 women with a mean age of 80 years and 47% black. Women reported birth weight and complications for each pregnancy. Analysis was limited to first births not complicated by hypertension or preeclampsia. RESULTS: Women who had delivered a first-birth infant weighing less than 2500 g had a lower body mass index (BMI) compared with women with a normal-weight (>or=2500 g) infant (26.7 versus 28.4 kg/m2; p=0.02), but they had a larger abdominal circumference for BMI (97.9 versus 95.5 cm; p=0.05). They also were marginally more likely to be administered antihypertensive medication (p=0.06). After adjustment for BMI, race, and age, women with a history of a small infant had elevations in systolic blood pressure (p=0.05) and greater IL-6 levels (p=0.02) and were more insulin resistant (p=0.05) compared with women with a normal-weight infant. CONCLUSIONS: These findings suggest that a history of LBW delivery identifies women with elevated cardiovascular risk factors.

Black or African American↗

PubMed2006

Hypertriglyceridemia and hypercholesterolemia in human immunodeficiency virus-1-infected children treated with protease inhibitors.

BACKGROUND: Adverse effects associated with highly active antiretroviral therapy (HAART), particularly protease inhibitors (PIs), have been identified in adult and pediatric patients. In this study, we monitored, for cholesterol and triglyceride levels, a cohort of HIV-1-infected children receiving a HAART regimen. METHODS: HIV-infected patients <17 years old belonging to a cohort that has been followed since 1997 were enrolled in the study. Patients were receiving either a three- or four-drug antiretroviral regimen that included two nucleoside reverse transcriptase inhibitors (lamivudine and zidovudine) combined with one or two PIs (ritonavir and/or saquinavir). Cholesterol and triglyceride levels were measured on fasting serum samples drawn at the time of enrollment and every 3 months thereafter. Clinical evaluation was performed on a monthly basis. RESULTS: Twenty four patients were included. Median age at HIV infection diagnosis was 15 months. Twenty one patients received a four-drug antiretroviral regimen, while three patients received ritonavir plus zidovudine and lamivudine. Median follow-up was 27 months; 62.5% of patients had hypercholesterolemia and 79.2% had hypertriglyceridemia, most typically after 15 months of treatment. None of the patients had physical changes in body fat distribution suggesting lipodystrophy. CONCLUSIONS: Hyperlipidemia is a frequent complication in HIV-1-infected children undergoing antiretroviral treatment that includes PIs. Additional studies with larger cohorts and a longer follow-up are needed to propose a rationale and alternatives for patients who develop dyslipidemia while receiving PIs.

Adolescent↗