Increased serum leptin level in overweight patients with colon carcinoma: A cross-sectional and prospective study

Wang, Di; Gao, Lichen; Gong, Kuiyu; Chai, Qin; Wang, Guihua

doi:10.3892/mco.2016.1087

Cited by 9 publications

(8 citation statements)

References 10 publications

(18 reference statements)

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“…Circulating leptin concentrations are known to reflect total body fat and to be higher in females than in males. In our patients, serum leptin in men and women did not differ, and its levels were comparable with those of control subjects in previous studies [33,34]. Leptin was lower in children, as could be expected.…”

Section: Discussionsupporting

confidence: 89%

Circulating brain-derived neurotrophic factor, leptin, neuropeptide Y, and their clinical correlates in cystic fibrosis: a cross-sectional study

Nowak

Szczepanik

Trypuć

et al. 2020

aoms

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Introduction: Cystic fibrosis (CF) involves chronic inflammation and decreased pulmonary function, which increase caloric demand. Yet, sufficient energy provision is hindered by reduced appetite and fat malabsorption. Brain-derived neurotrophic factor (BDNF), leptin, and neuropeptide Y (NPY) belong to energy balance-regulating factors. We aimed to assess their concentrations in CF patients in order to search for potential clinical correlates. Material and methods: This was an exploratory, cross-sectional study. Patients' weight and height Z-scores, forced expiratory volume in 1 s (FEV 1 %), exocrine pancreatic status (fecal elastase-1), genotypes, and other characteristics were assessed. Serum concentrations of BDNF, leptin, NPY, IL-6, and TNF-α were measured using ELISA. Results: The study enrolled 56 patients, of whom 29 (52%) were female and 17 (30%) were younger than 16 years. Median (1 st-3 rd quartile) mass Z-score was-0.85 (-1.56-(-0.36)); median FEV 1 was 70.5% (45.0-89.5); 48 (86%) patients had exocrine pancreatic insufficiency and 8 (14%) diabetes. Overall, median concentrations were: BDNF: 33.91 ng/ml (26.40-40.43), leptin: 12.05 ng/ml (8.93-17.77), NPY: 2.86 ng/ml (1.75-4.42). None of these factors correlated with mass Z-score, FEV 1 %, IL-6 or TNF-α. Leptin and NPY correlated negatively (ρ =-0.62, p = 3 × 10-7); BDNF/NPY ratio was associated with leptin (ρ = 0.54, p = 2 × 10-5), BDNF/leptin ratio correlated with NPY (ρ = 0.60, p = 1 × 10-6). In a multivariable regression analysis NPY was weakly, but independently, associated with FEV 1 %, and leptin with age. Conclusions: BDNF and leptin were not associated with weight Z-score or FEV 1 %. Serum NPY concentrations seemed to be lower in CF patients with reduced pulmonary function independently of malnutrition and inflammation.

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Section: Discussionsupporting

confidence: 89%

Circulating brain-derived neurotrophic factor, leptin, neuropeptide Y, and their clinical correlates in cystic fibrosis: a cross-sectional study

Nowak

Szczepanik

Trypuć

et al. 2020

aoms

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“…In a study on 30 patients with colorectal, breast, lung, testicular or gastric cancer, no significant differences were observed in the serum leptin level at baseline or in response to chemotherapy between patients and matched healthy controls, although leptin was identified to be positively associated with the body mass index of patients (27). By contrast, when focusing on a specific type of cancer, several studies suggest a positive association between higher serum leptin level and cancers (28,29), while some suggest a negative correlation (11,30). Meta-analysis revealed that obesity is a risk factor for cholangiocarcinoma (31).…”

Section: Discussionmentioning

confidence: 97%

Leptin stimulates the epithelial‑mesenchymal transition and pro‑angiogenic capability of cholangiocarcinoma cells through the miR‑122/PKM2 axis

Peng

Sun

et al. 2019

Int J Oncol

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Leptin is an adipokine minimally known for its activities or underlying mechanisms in cholangiocarcinoma. The present study explored the effects of leptin on the epithelial-mesenchymal transition (EMT) and pro-angiogenic capability of cholangiocarcinoma cells, and investigated the underlying mechanisms. Cholangiocarcinoma cells were treated with leptin, and their migration and invasion rates were investigated using Transwell assays. Furthermore, conditioned medium was collected from cholangiocarcinoma cells following leptin treatment and applied to human umbilical vein endothelial cells to assess tube formation. The expression of EMT and pro-angiogenic factors was examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analyses. Mechanistically, the function of pyruvate kinase muscle isozyme M2 (PKM2) was assessed in leptin-induced phenotypes using siRNA targeting PKM2 (si-PKM2). Bioinformatics screening and luciferase reporter assays were used to reveal microRNA (miR)-122 as the potential mediator between leptin and PKM2. Finally, the associations between leptin and miR-122 or PKM2 levels in patients with cholangiocarcinoma were assessed by ELISA and RT-qPCR. Leptin significantly increased the EMT and pro-angiogenic capability of cholangiocarcinoma cells, visibly inhibited endogenous miR-122 expression, and upregulated PKM2. Furthermore, si-PKM2 inhibited leptin-induced migration, invasion, EMT-associated marker expression levels and the pro-angiogenic capability in cholangiocarcinoma cells. In addition, miR-122 negatively regulated the expression of PKM2. When applied together with leptin, miR-122 was sufficient to reverse the multiple malignancy-promoting effects of leptin. Consistently, the serum leptin level positively correlated with that of PKM2, but negatively with that of miR-122 in patients with cholangiocarcinoma. Leptin, by downregulating miR-122 and elevating PKM2 expression, acts as a pleiotropic pro-malignancy cytokine for cholangiocarcinoma. Therefore, increasing miR-122 expression and inhibiting PKM2 may be future approaches for cholangiocarcinoma treatment.

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“…Even leptin gene variants could exhibit sex-specific associations with CRC risk [ 119 ]. Moreover, serum leptin levels have been demonstrated to decrease following colectomy, supporting the association between leptin and CRC [ 120 ], thus suggesting leptin/Ob-R as a good target in the prevention and treatment of CRC, especially for obese patients [ 121 ].…”

Section: Role Of Leptin As a Bad Actor In Cancermentioning

confidence: 99%

Leptin, Both Bad and Good Actor in Cancer

Jiménez‐Cortegana¹,

López-Saavedra²,

Sánchez-Jiménez³

et al. 2021

Biomolecules

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Leptin is an important regulator of basal metabolism and food intake, with a pivotal role in obesity. Leptin exerts many different actions on various tissues and systems, including cancer, and is considered as a linkage between metabolism and the immune system. During the last decades, obesity and leptin have been associated with the initiation, proliferation and progression of many types of cancer. Obesity is also linked with complications and mortality, irrespective of the therapy used, affecting clinical outcomes. However, some evidence has suggested its beneficial role, called the “obesity paradox”, and the possible antitumoral role of leptin. Recent data regarding the immunotherapy of cancer have revealed that overweight leads to a more effective response and leptin may probably be involved in this beneficial process. Since leptin is a positive modulator of both the innate and the adaptive immune system, it may contribute to the increased immune response stimulated by immunotherapy in cancer patients and may be proposed as a good actor in cancer. Our purpose is to review this dual role of leptin in cancer, as well as trying to clarify the future perspectives of this adipokine, which further highlights its importance as a cornerstone of the immunometabolism in oncology.

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Increased serum leptin level in overweight patients with colon carcinoma: A cross-sectional and prospective study

Cited by 9 publications

References 10 publications

Circulating brain-derived neurotrophic factor, leptin, neuropeptide Y, and their clinical correlates in cystic fibrosis: a cross-sectional study

Circulating brain-derived neurotrophic factor, leptin, neuropeptide Y, and their clinical correlates in cystic fibrosis: a cross-sectional study

Leptin stimulates the epithelial‑mesenchymal transition and pro‑angiogenic capability of cholangiocarcinoma cells through the miR‑122/PKM2 axis

Leptin, Both Bad and Good Actor in Cancer

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