Curcumin, a natural bioactive compound, is known to exert therapeutic effects on cancer and dysplasia. However, less is known about its effects on DNA damage and repair in obesity. Therefore, this study was to examine the novel role of curcumin in regulating DNA repair signalling using a high-fat diet (HFD)-induced obesity in mice. Male C57BL/6 mice were fed either a 60 % HFD or standard chow with curcumin (2·5 g/kg diet) for 8 weeks. We observed that curcumin alleviated weight gain, preserved glucose balance and enhanced liver fat accumulation and lipid profile in mice with obesity induced by an HFD. Curcumin enhanced the adipocyte-derived mesenchymal stem cell (ADMSC) population (Sca-1 + CD45-) and expression of phosphorylated checkpoint kinase1 (pCHK1), a DNA repair gene, in adipocytes isolated from adipose tissues of HFD-induced obesity in mice. Moreover, in human preadipocytes, treatment with 10 μM curcumin effectively reduced the mRNA levels of IL6 and CCL2 in a dose-dependent manner, while treatment with 100 μM H2O2 together with curcumin upregulated the levels of pCHK2 and total CHK2 protein and reduced level of γH2AX, a biomarker of DNA damage. In addition, curcumin inhibits preadipocyte-to-adipocyte differentiation. In conclusion, our data demonstrated that curcumin reduced the pro-inflammatory response and DNA damage in adipocytes, controlling weight gain in mice with HFD-induced obesity.

The therapeutic effects of soya consumption on adipokine concentrations have yielded inconsistent results in previous meta-analyses. This umbrella meta-analysis aims to investigate the impact of soya and its isoflavones on serum adiponectin and leptin levels in adults. We searched the Cochrane Central, Web of Science, PubMed and Scopus databases until October 10, 2024. The articles were restricted to those written in English. We included meta-analysis studies that evaluated the effects of soya and its isoflavones on levels of adiponectin and leptin and reported effect sizes (ES) and corresponding CI. Two independent reviewers screened all articles based on eligibility criteria and extracted the required data from the included meta-analyses. The meta-analysis was performed using a random-effects model in STATA software. Six meta-analyses of randomised controlled trials meeting the inclusion criteria were included in the current umbrella meta-analysis. The findings indicated that soya and its isoflavones did not have a significant effect on adiponectin (ES = 0·10; 95 % CI: −0·22, 0·41; P = 0·55; I2 = 51·8 %) and leptin (ES = −0·37; 95 % CI: −1·35, 0·61; P = 0·46; I2 = 71·2 %) concentrations. Subgroup analysis based on participants’ mean age, total sample size and duration was conducted. Results showed that the effect is not statistically significant in any of the subgroups. In conclusion, soya and its isoflavones could not improve the adipokines mentioned above. However, further high-quality research in different countries is required to substantiate these findings.

Breast milk (BM) is the only source of iodine and bioactive compounds that influence growth and development in infants. The content of BM may be influenced by maternal body mass index (BMI). The aim of this study was to investigate the effect of maternal weight on BM and cord blood iodine concentrations, growth-related hormones, infant anthropometric measurements. A total of 84 mother-infant pairs participated. Levels of leptin, adiponectin and insulin-like growth factor-I (IGF-I) in postnatal BM and cord blood were analysed by enzyme-linked immunosorbent assay (ELISA), iodine by Sandell-Kolthoff reaction. Dietary iodine intake of women was determined by food frequency questionnaire, and anthropometric measurements of infants at birth and 3 months were evaluated. Dietary iodine intake was found to be similar in normal weight (NW) and overweight/obese (OW/OB) women (p > 0.05). Breast milk iodine concentration (BMIC) was 17.4 μg in NW, 18.2 μg in OB/OW women. Adiponectin in cord blood and IGF-I in BM were higher OB/OW than NW women (p < 0.05). Positive correlations were found between the infant birth weight and adiponectin in BM, between the infant body weight at 3 months and leptin and adiponectin in BM, between the infant birth head circumference and IGF-I in BM (p < 0.05). In multiple linear regression model, leptin and adiponectin in BM had a positive effect on infant body weight (p < 0.05). Maternal BMI may influence infant body weight via leptin and adiponectin in BM and infant head circumference via IGF-I. No relationship was found between maternal BMI and iodine levels and anthropometric measurements of the infant. Longitudinal studies are recommended to understand the effect of BMIC on growth.

Milk fat synthesis is tightly regulated by hormones and growth factors. Leptin is a versatile peptide hormone that exerts pleiotropic effects on metabolic pathways. In this study, we evaluated the expression and function of leptin and its long form receptor OB-Rb in dairy cow mammary tissues from different physiological stages and in cultured mammary epithelial cells. The results showed that the expression of leptin and OB-Rb were significantly higher in the mammary tissues of lactating cows as compared with dry cows, suggesting that they are related to milk component synthesis. In cultured dairy cow mammary epithelial cells, leptin treatment significantly increased OB-Rb expression and intracellular triacylglycerol content. Transcriptome analysis identified the difference in gene expression between leptin treated cells and control cells, and 317 differentially expressed genes were identified. Gene ontology and pathway mapping showed that lipid metabolism-related gene expression increased and signal transduction pathway-related genes were the most significantly enriched. Mechanistic studies showed that leptin stimulation enhanced sterol regulatory element-binding protein 1 expression via activating the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway, which in turn up-regulated the expression of genes related to milk fat synthesis. Moreover, we found that fatty acid synthesis precursors, acetate and β-hydroxybutyrate, could positively regulate the expression of leptin and OB-Rb in bovine mammary epithelial cells, thereby potentially increasing milk fat synthesis. Our study provided novel evidence in the regulation of leptin on milk fat production in mammary glands of dairy cows, as well as experimental basis for artificial regulation of milk fat

Curcumin is a phytocompound found in the root of turmeric, a common herbal ingredient in many Asian cuisines. The compound contains anti-inflammatory activity, which is mediated through an upregulation of adiponectin and reduction of leptin. Results of randomised controlled trials (RCT) have shown that the effects of curcumin on adipokines are conflicting. Therefore, the current systematic review and meta-analysis of RCT were conducted with the aim of elucidating the role of curcumin supplementation on serum adiponectin and leptin. The search included PubMed, Embase, Cochrane Library, Scopus, Web of Science and Google Scholar from inception to August 2023. For net changes in adipokines, standardised mean differences (SMD) were calculated using random effects models. Thirteen RCT with fourteen treatment arms were eligible for inclusion in this meta-analysis. Curcumin supplementation was effective in increasing serum adiponectin (SMD = 0·86, 95 % CI (0·33, 1·39), P < 0·001; I2 = 93·1 %, P < 0·001) and reducing serum leptin (SMD = −1·42, 95 % CI (−2·29, −0·54), P < 0·001; I2 = 94·7 %, P < 0·001). In conclusion, curcumin supplementation significantly increased circulating adiponectin and decreased leptin levels in adults.

This study aimed to investigate the effect of leptin gene polymorphism and some environmental factors on milk production traits. Blood samples from 212 Holstein Friesian dairy cattle reared on a private farm were used. The intron 2 region of the leptin gene was digested with Sau3AI restriction enzyme using the PCR-RFLP method. A and B alleles and AA, AB, and BB genotype frequencies for the Sau3AI polymorphism were determined as 0.8821 and 0.1179, and 0.764, 0.236 and 0.000, respectively. Chi-square analysis revealed that the leptin gene polymorphism followed the Hardy–Weinberg equilibrium, including the absence of animals with the BB genotype. The effect of leptin gene polymorphism on all milk production traits was insignificant. For milk production traits, direct heritability (ha2) varied between 0.03 ± 0.283 (for the dry period) and 0.50 ± 0.183 (for milk conductivity). Regarding the milking time (MT), the estimated breeding values (EBVs) of cattle with the AA genotype were higher than the AB genotype (P < 0.05). As a result of this study, in the selection program, allele or genotype could not be suggested as a marker for milk yield characteristics except for the possible exception of milking time and its relationship to mastitis incidence.

Research suggests that adiponectin, leptin, and genetic polymorphisms such as catechol-O-methyltransferase (COMT) genotype may play an integral role in blood pressure status and thereby cardiovascular health. This is an area especially important for women who are post-menopause; however, the current literature investigating these associations is limited. This study was a cross-sectional secondary analysis of baseline data (N 237) from the Minnesota Green Tea Trial (MGTT). The current study explored the relationships between plasma adiponectin, leptin, and COMT genotype on blood pressure measures. Plasma adiponectin and leptin were obtained after an overnight fast of at least 10 h and were measured by the radioimmunoassay method. The relationships were analysed using multiple linear regression after adjusting for potential confounders. Effect modifications by age, body mass index (BMI) category, blood pressure category, antihypertensive medication use, and COMT genotype were also investigated. The majority of participants were non-Hispanic (97⋅9 %) and Caucasian (94⋅9 %). Mean (sd) age and BMI were 60⋅7 (5⋅0) years and 28⋅2 (2⋅9) kg/m2, respectively. After adjustment for confounding variables, neither plasma adiponectin, plasma leptin nor COMT genotype was associated with systolic or diastolic blood pressure measures. The results of stratified analyses also did not reveal any significant interactions or associations. Based on the findings of this study, which utilised more rigorous statistical methods than previous research, neither adiponectin, leptin nor COMT genotype play a role in blood pressure measures in women who are post-menopause.

Inflammation and immune evasion are major key players in breast cancer (BC) progression. Recently, the FDA approved the use of anti-programmed death-ligand 1 antibody (anti-PD-L1) and phosphoinositide 3-kinase (PI3K) inhibitors against aggressive BC. Despite the paradigm shift in BC treatments, patients still suffer from resistance, recurrence and serious immune-related adverse events. These obstacles require unravelling of the hidden molecular contributors for such therapy failure hence yielding therapeutics that are at least as efficient yet safer. Inflammasome pathway is activated when the pattern recognition receptor senses danger signals (danger-associated molecular patterns) from damagedRdying cells or pathogen-associated molecular patterns found in microbes, leading to secretion of the active pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18). It has been shown throughout numerous studies that inflammasome pathway enhanced invasion, metastasis, provoked BC progression and therapy resistance. Additionally, inflammasomes upregulated the proliferative index ki67 and enhanced PD-L1 expression leading to immunotherapy resistance. IL-1β contributed to significant decrease in oestrogen receptor levels and promoted BC chemo-resistance. High levels of IL-18 in sera of BC patients were associated with worst prognosis. Stimulation of purinergic receptors and modulation of adipokines in obese subjects activated inflammasomes that evoked radiotherapy resistance and BC progression. The micro RNA miR-223-3p attenuated the inflammasome over-expression leading to lowered tumour volume and lessened angiogenesis in BC. This review sheds the light on the molecular pathways of inflammasomes and their impacts in distinct BC subtypes. In addition, it highlights novel strategies in treatment and prevention of BC.

Breast milk leptin plays a potential role in preventing childhood obesity. However, the associations of breast milk leptin with maternal metabolism in pregnancy and dietary patterns during lactation are still unclear. We aimed to explore associations of breast milk leptin with maternal metabolic profiles in pregnancy and dietary patterns during lactation. A total of 332 participants were recruited for this retrospective cohort study. Breast milk samples were collected at approximately 6 weeks postpartum. Breast milk leptin and twenty-three metabolic profiles in pregnancy were measured in this study. A semi-quantitative FFQ was used to gather dietary information during lactation. Both principal component analysis and the diet balance index were used to derive dietary patterns. Among twenty-three maternal metabolic profiles, maternal serum glucose (β = 1·61, P = 0·009), γ-glutamyl transferase (β = 0·32, P = 0·047) and albumin (β = −2·96, P = 0·044) in pregnancy were correlated with breast milk leptin. All dietary patterns were associated with breast milk leptin. Given the joint effects of maternal metabolism in pregnancy and dietary patterns during lactation, only diet quality distance was significantly associated with leptin concentrations in breast milk (low level v. almost no diet problem: β = −0·46, P = 0·011; moderate/high level v. almost no diet problem: β = −0·43, P = 0·035). In conclusion, both maternal metabolism in pregnancy and dietary patterns during lactation were associated with breast milk leptin. Maternal diet balance during lactation was helpful to improve breast milk leptin concentration.

I had been working on the endocrine and signalling role of white adipose tissue (WAT) since 1994 following the identification of the ob (Lep) gene(1), this after some 15 years investigating the physiological role of brown adipose tissue. The ob gene, a mutation in which it is responsible for the profound obesity of ob/ob (Lepob/Lepob) mice, is expressed primarily in white adipocytes and encodes the pleiotropic hormone leptin. The discovery of this adipocyte hormone had wide-ranging implications, including that white fat has multiple functions that far transcend the traditional picture of a simple lipid storage organ.

Protein quality has an important role in increasing satiety. Evidence suggests that whey protein (WP) provides satiety via gastrointestinal hormone secretion. Hydrolysed collagen supplementation can also stimulate the production of incretins and influence satiety and food intake. Thus, we sought to compare the effect of acute supplementation of WP or hydrolysed collagen on post-intervention appetite and energy consumption. This was a randomised, double-blind, crossover pilot study with ten healthy adult women (22·4 years/old) who were submitted to acute intake (single dose) of a beverage containing WP (40 g of concentrated WP) or hydrolysed collagen (40 g). Subjective appetite ratings (feelings of hunger, desire to eat and full stomach) were measured using the Visual Analog Scale (VAS), energy intake was quantified by ad libitum cheese bread consumption 2 hours after supplementation and blood was collected for leptin and glucose determination. There was no difference between treatment groups in the perception of hunger (P = 0·983), desire to eat (P = 0·326), full stomach feeling (P = 0·567) or food consumption (P = 0·168). Leptin concentrations at 60 min post supplementation were higher when subjects received hydrolysed collagen (P = 0·006). Acute supplementation with hydrolysed collagen increased leptin levels in comparison with WP, but had no effect on appetite measured by feelings of hunger, desire to eat, full stomach feeling (VAS) or energy consumption.

Literature reports that insults, such as hormonal disturbances, during critical periods of development may modulate organism physiology and metabolism favoring cardiovascular diseases (CVDs) later in life. Studies show that leptin administration during lactation leads to cardiovascular dysfunction in young and adult male Wistar rats. However, there are sex differences regarding CVD. Thus, the present work aimed to investigate neonatal leptin administration’s consequences on different outcomes in female rats at prepubertal and adult age. Newborn Wistar female rats were divided into two groups, Leptin and Control, receiving daily subcutaneous injections of this adipokine (8 μg/100 g) or saline for the first 10 of 21 d of lactation. Nutritional, biometric, hemodynamic, and echocardiographic parameters, as well as maximal effort ergometer performance, were determined at postnatal days (PND) 30 and 150. Leptin group presented lower food intake (p = 0.0003) and higher feed efficiency (p = 0.0058) between PND 21 and 30. Differences concerning echocardiographic parameters revealed higher left ventricle internal diameter (LVID) in systole (p = 0.0051), as well as lower left ventricle ejection fraction (LVEF) (p = 0.0111) and fractional shortening (FS) (p = 0.0405) for this group at PND 30. Older rats treated with leptin during lactation presented only higher LVID in systole (p = 0.0270). Systolic blood pressure and maximum effort ergometer test performance was similar between groups at both ages. These data suggest that nutritional, biometric, and cardiac outcomes due to neonatal leptin administration in female rats are age-dependent.

The double burden of malnutrition (DBM) has been described in many low-/middle-income countries. We investigated food addiction, thyroid hormones, leptin, the lipid/glucose profile and body composition in DBM children/adolescents. Subjects were allocated into groups according to nutritional status: control (C, n 28), weight excess (WE, n 23) and DBM (WE plus mild stunting, n 22). Both the DBM and WE groups showed higher mean insulin concentrations than the control (DBM = 57·95 (95 % CI 47·88, 70·14) pmol/l, WE = 74·41 (95 % CI 61·72, 89·80) pmol/l, C = 40·03 (95 % CI 34·04, 47·83) pmol/l, P < 0·001). WE and DBM showed more food addiction symptoms than the control (3·11 (95 % CI 2·33, 3·89), 3·41 (95 % CI 2·61, 4·20) and 1·66 (95 % CI 0·95, 2·37)). In DBM individuals, addiction symptoms were correlated with higher body fat and higher insulin and leptin levels. These data provide preliminary evidence consistent with the suggestion that DBM individuals have a persistent desire to eat, but further studies are required to confirm these results in a larger study. These hormonal changes and high body fat contribute to the development of diabetes in long term.

Respiratory distress syndrome results from inadequate functional pulmonary surfactant and is a significant cause of mortality in preterm infants. Surfactant is essential for regulating alveolar interfacial surface tension, and its synthesis by Type II alveolar epithelial cells is stimulated by leptin produced by pulmonary lipofibroblasts upon activation by peroxisome proliferator-activated receptor γ (PPARγ). As it is unknown whether PPARγ stimulation or direct leptin administration can stimulate surfactant synthesis before birth, we examined the effect of continuous fetal administration of either the PPARγ agonist, rosiglitazone (RGZ; Study 1) or leptin (Study 2) on surfactant protein maturation in the late gestation fetal sheep lung. We measured mRNA expression of genes involved in surfactant maturation and showed that RGZ treatment reduced mRNA expression of LPCAT1 (surfactant phospholipid synthesis) and LAMP3 (marker for lamellar bodies), but did not alter mRNA expression of PPARγ, surfactant proteins (SFTP-A, -B, -C, and -D), PCYT1A (surfactant phospholipid synthesis), ABCA3 (phospholipid transportation), or the PPARγ target genes SPHK-1 and PAI-1. Leptin infusion significantly increased the expression of PPARγ and IGF2 and decreased the expression of SFTP-B. However, mRNA expression of the majority of genes involved in surfactant synthesis was not affected. These results suggest a potential decreased capacity for surfactant phospholipid and protein production in the fetal lung after RGZ and leptin administration, respectively. Therefore, targeting PPARγ may not be a feasible mechanistic approach to promote lung maturation.