The Role of Leptin in Systemic Lupus Erythematosus: Is It Still a Mystery?

Villa, Nicole; Badla, Omar; Goit, Raman; Saddik, Samia E; Dawood, Sarah N; Rabih, Ahmad M; Mohammed, Ahmad; Raman, Aishwarya; Uprety, Manish; Calero, Maria Jose; Villanueva, Maria Resah B; Joshaghani, Narges; Mohammed, Lubna

doi:10.7759/cureus.26751

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…Numerous studies, including observational studies, clinical trials, and animal experiments have been performed to examine the association between adipokine levels and SLE risk. As mentioned, above however, the existing studies [4][5][6][7][8][9][10][11][12] on the associations between the three major adipokines and SLE have shown inconsistent results; some support null associations while others support significantly correlated relationships. Since the observational studies are usually subject to confounding effects (either unobserved or unadjusted) and reverse causality, especially for retrospective studies, the positive findings of these previous studies should be interpreted with caution.…”

Section: Discussionmentioning

confidence: 98%

“…Leptin levels are highly correlated with adiposity, a commonly known risk factor for a variety of complex diseases such as diabetes, certain cancer types, and cardiovascular disease [3]. To date, observational studies and meta-analyses [4][5][6][7] have shown that compared to healthy controls, serum/plasma leptin levels are elevated in patients with SLE and tend to increase with disease severity. Furthermore, a review article [8] discussed the pathogenic mechanism of leptin in SLE to provide insights into the development of leptin-based approaches for the treatment of SLE.…”

Section: Introductionmentioning

confidence: 99%

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Mendelian randomization analyses reveal no genetic causal effects of major adipokines on systemic lupus erythematosus

Duan,

Tian

2024

PLoS ONE

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Epidemiological studies have shown that the levels of serum adipokine such as leptin and resistin are associated with the risk of developing systemic lupus erythematosus (SLE). Nevertheless, whether either leptin or resistin has causal impacts on the risk of SLE is still unknown. In this study, two-sample univariable MR analyses and multivariable MR analysis were performed to explore the causal relationships between adipokines and SLE. Additionally, the potential causal effects of SLE on major adipokines were evaluated using reverse MR analyses. The results of inverse-variance weighted (IVW), weighted median, weighted mode and MR‒Egger methods concordantly supported that major adipokines have no causal effects on the risk of SLE. In the multivariable MR IVW analysis with leptin and resistin as covariates, neither leptin (odds ratio (OR) = 3.093, P = 0.067) nor resistin (OR = 0.477, P = 0.311) was identified as an independent risk factor for SLE, which is in line with the univariable MR results. In conclusion, our analyses revealed no evidence to support that these three major adipokines are risk factors for SLE.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Mendelian randomization analyses reveal no genetic causal effects of major adipokines on systemic lupus erythematosus

Duan,

Tian

2024

PLoS ONE

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“…Leptin is involved in low-grade inflammation due to overweight and obesity and is considered a proinflammatory adipokine [44]. In SLE patients, leptin is highly produced; however, it does not correlate with disease activity [45].…”

Section: Cytokines and Adipokines In Sle Along With Metsmentioning

confidence: 99%

Biomarkers in Systemic Lupus Erythematosus along with Metabolic Syndrome

Corona-Meraz,

Vázquez-Del Mercado,

Sandoval-García

et al. 2024

JCM

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Metabolic syndrome (MetS) is a group of physiological abnormalities characterized by obesity, insulin resistance (IR), and hypertriglyceridemia, which carry the risk of developing cardiovascular disease (CVD) and type 2 diabetes (T2D). Immune and metabolic alterations have been observed in MetS and are associated with autoimmune development. Systemic lupus erythematosus (SLE) is an autoimmune disease caused by a complex interaction of environmental, hormonal, and genetic factors and hyperactivation of immune cells. Patients with SLE have a high prevalence of MetS, in which elevated CVD is observed. Among the efforts of multidisciplinary healthcare teams to make an early diagnosis, a wide variety of factors have been considered and associated with the generation of biomarkers. This review aimed to elucidate some primary biomarkers and propose a set of assessments to improve the projection of the diagnosis and evolution of patients. These biomarkers include metabolic profiles, cytokines, cardiovascular tests, and microRNAs (miRs), which have been observed to be dysregulated in these patients and associated with outcomes.

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“…р К-У =0,0005 Частота ИР нарастала от 1 (3%) случая при «нормальном весе» до 4 (18%) при «скрытом» и 10 (29%) при «классическом» фенотипе (р=0,009 при сравнении с «нормальным весом»). Продемонстрировано постепенное увеличение доли пациентов, получавших гипотензивные препараты: от 2 (6%) при «нормальном весе» до 10 (45%) при «скрытом» фенотипе (р=0,0012 при сравнении с «нормальным весом») и до 23 В зарубежной и отечественной литературе не найдено сведений о сравнении концентрации лептина при РА и СКВ, хотя существуют сообщения как о повышенных, так и о сходных уровнях адипоцитокина при этих ИВРЗ по сравнению со здоровым контролем [26][27][28][29]. В ряде работ частота ИР при РА оказалась больше, чем при СКВ [33,34], а в других исследованиях она была сопоставима [35,36].…”

Section: а бunclassified

“…Уровень лептина прямо коррелирует с толщиной интимамедиа сонных и кальцификацией коронарных артерий, прогрессированием атеросклероза, СН и тяжелым течением ИБС [19][20][21][22][23][24][25]. Данные об уровне лептина при РА и СКВ, а также о его взаимосвязи с метаболическими нарушениями противоречивы [26][27][28][29].…”

unclassified

Hyperleptinemia as a marker of various phenotypes of obesity and overweight in women with rheumatoid arthritis and systemic lupus erythematosus

Kondratyeva¹,

Gorbunova²,

Panafidina³

et al. 2023

Naučno-praktičeskaâ revmatologiâ

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Objective – to identify different phenotypes of overweight in women with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) based on body mass index (BMI) and serum leptin levels, as well as to determine the frequencies of various metabolic disorders, hypertension and cardiovascular complications in individual phenotypes. Material and methods. The study included 50 women with RA and 46 with SLE aged 18 to 65 years without a history of diabetes and fasting hyperglycemia. The concentration of leptin (ELISA), insulin (electrochemiluminescence analysis) was determined in all patients, and the HOMA-IR index was calculated. Hyperleptinemia was diagnosed at leptin concentrations >11,1 ng/ml, insulin resistance (IR) – at HOMA-IR values ≥2,77. Three main phenotypes of overweight were distinguished: “classic” (BMI≥25 kg/m2 + hyperleptinemia), “healthy” (BMI≥25 kg/m2 , without hyperleptinemia), “hidden” or “latent” (BMI<25 kg/m2 + hyperleptinemia), as well as “normal weight” (BMI<25 kg/m2 , without hyperleptinemia). Results. Patients with RA and SLE were similar in age (p=0.4), disease duration (p=0.2) and BMI (p=0.5). Hyperleptinemia was found in 46% of women with RA and 74% – with SLE (p=0.005), IR – in 10% and 22% of patients, respectively (p=0.2). The “classic” phenotype of overweight was diagnosed in 30%, “healthy” – in 8%, “hidden” – in 16% of cases with RA and in 44%, 0% and 30% of cases with SLE, respectively. IR was found in 3%, hypertension – in 6% of patients with “normal weight”. With the “classical” phenotype, IR (29%) and hypertension (66%) were more common than with “normal weight” (p<0.01 in all cases), with the “hidden” phenotype, significant differences were obtained only in hypertension frequency (45%; p=0.0012), but not IR (18%). 3 out of 4 women with a history of cardiovascular complications suffered from “classic” overweight, one patient had a “normal weight”. Conclusion. In women with SLE up to 65 years of age, the frequency of hyperleptinemia, but not IR, is higher than in patients with RA. In both diseases, the “classic” overweight phenotype is most common. In RA, a “hidden” phenotype was detected less often than in SLE, at the same time, a “healthy” phenotype is not characteristic of SLE. The frequencies of metabolic disorders and hypertension is low with the “normal weight” and “healthy” phenotype, high – with the “classic”, intermediate – with the “hidden” phenotype.

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The Role of Leptin in Systemic Lupus Erythematosus: Is It Still a Mystery?

Cited by 4 publications

References 28 publications

Mendelian randomization analyses reveal no genetic causal effects of major adipokines on systemic lupus erythematosus

Mendelian randomization analyses reveal no genetic causal effects of major adipokines on systemic lupus erythematosus

Biomarkers in Systemic Lupus Erythematosus along with Metabolic Syndrome

Hyperleptinemia as a marker of various phenotypes of obesity and overweight in women with rheumatoid arthritis and systemic lupus erythematosus

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