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.

Previous nutritional studies have shown that insulin regulation is different between DT and A strains of gibel carp. As leptin plays a pivotal role in the effects of insulin, we hypothesised that leptin regulation of glucose and lipid metabolism would differ between the two strains. To test our hypothesis, recombinant human leptin was injected into two strains. The results showed that leptin activated the phosphatidylinositol 3-kinase (PI3K)–protein kinase B (AKT), AMP-activated protein kinase–acetyl coenzyme A carboxylase and Janus kinase 2 (JAK2)–signal transducer and activator of transcription (STAT) signalling pathways in both strains. Hypoglycaemia induced by leptin might be due to higher glucose uptake by the liver and muscles together with enhanced glycolytic potential and reduced gluconeogenic potential. Decreased lipogenesis and up-regulated fatty acid oxidation were induced by leptin. In terms of genotype, the PI3K–AKT signalling pathway was more strongly activated by leptin in the muscle tissue of the A strain, as reflected by the heightened phosphorylation of AKT. Furthermore, glycogen content, glycolytic enzyme activity and gluconeogenic capability were higher in the A strain than the DT strain. Strain A had higher levels of fatty acid synthesis and lipolytic capacity in the liver than the DT strain, but the opposite was true in white muscle. Regarding leptin–genotype interactions, the DT strain displayed stronger regulation of glucose metabolism in the liver by leptin as compared with the A strain. Moreover, a more active JAK2–STAT signalling pathway accompanied by enhanced inhibition of fatty acid synthesis by leptin was observed in the DT strain. Overall, the regulation of glucose and lipid metabolism by leptin differed between the two strains, as expected.

Excess body weight confers a high risk to human health. Body weight variation between subjects can be partially explained by genetic differences. The aim of the present study was to investigate the association of genetic variants in the ADIPOQ (rs2241766) and LEP (rs7799039) genes with body weight trajectories in children from birth to 6 years of age. This was a prospective cohort (PREDI Study). Socio-economic, biological and anthropometric data were collected at four time points: at birth in the maternity unit; 1–2, 4–5 and 6 years old at the participants’ homes. Genotyping was performed by PCR-restriction fragment length polymorphism. Poisson regression and linear mixed-effect regression models were used to address the association of ADIPOQ and LEP genotypes with BMI. Excessive body weight at pre-pregnancy (β = 0·339, P = 0·01) and excessive gestational weight gain (β = 0·51, P < 0·001) were associated with children’s BMI trajectory from birth to 6 years. The ADIPOQ-rs2241766 TG or GG genotype was associated with a higher risk of excess body weight in the first 6 years of life (both sexes relative risk 1·25, 95 % CI 1·01, 1·56; female relative risk 1·67, 95 % CI 1·20, 2·31). BMI increased over the years according to the presence of the TG or GG genotype (β = 0·01, 95 % CI 0·01, 0·02), particularly in females (β = 0·02, 95 % CI 0·01, 0·04). The ADIPOQ-rs2241766 TG and GG genotypes increased the risk of excess body weight in children from birth to 6 years of age and had a positive effect on body weight trajectories in girls. The LEP-rs7799039 genetic variant was not associated with body weight trajectory in children.

Rodents with mutations in the leptin, or leptin receptor, genes have been extensively used to investigate the regulation of energy balance and the factors that underlie the development of obesity. The excess energy gain of these mutants has long been considered as being due in part to increased metabolic efficiency, consequent to reduced energy expenditure, but this view has recently been challenged. We argue, particularly though not exclusively, from data on ob/ob mice, that three lines of evidence support the proposition that reduced expenditure is important in the aetiology of obesity in leptin pathway mutants (irrespective of the genetic background): (i) milk intake is similar in suckling ob/ob and +/? mice; (ii) ob/ob mice deposit excess energy when pair-fed to the ad libitum food intake of lean siblings; (iii) in several studies mutant mice have been shown to exhibit a lower RMR ‘per animal’ at temperatures below thermoneutrality. When metabolic rate is expressed ‘per unit body weight’ (inappropriately, because of body composition differences), then it is invariably lower in the obese than the lean. It is important to differentiate the causes from the consequences of obesity. Hyperphagic, mature obese animals weighing 2–3 times their lean siblings may well have higher expenditure ‘per animal’, reflecting the costs of being larger and of enhanced obligatory diet-induced thermogenesis resulting from the increased food intake. This cannot, however, be used to inform the aetiology of their obesity.

Early growth pattern is increasingly recognized as a determinant of later obesity. This study aimed to identify the association between weight gain in early life and anthropometry, adiposity, leptin, and fasting insulin levels in adolescence. A cross-sectional study was conducted in 366 school children aged 11–13 years. Weight, height, and waist circumference (WC) were measured. Fat mass (FM) was assessed using bioelectrical impedance analysis. Blood was drawn after a 12-h fast for insulin and leptin assay. Birth weight and weight at 6 months and at 18 months were extracted from Child Health Development Records. An increase in weight SD score (SDS) by ≥0.67 was defined as accelerated weight gain. Linear mixed-effects modeling was used to predict anthropometry, adiposity, and metabolic outcomes using sex, pubertal status, accelerated weight gain as fixed factors; age, birth weight, and family income as fixed covariates, and school as a random factor. Children with accelerated weight gain between birth and 18 months had significantly higher body mass index (BMI) SDS, WC SDS, height SDS, %FM, fat mass index (FMI), fat free mass index (FFMI), and serum leptin levels in adolescence. Accelerated weight gain between 6 and 18 months was associated with higher BMI SDS, WC SDS, %FM, and FMI, but not with height SDS or FFMI. Accelerated weight gain at 0–6 months, in children with low birth weight, was associated with higher height SDS, BMI SDS, WC SDS, %FM, and FMI; in children with normal birth weight, it was associated with BMI SDS, WC SDS, height SDS, and FFMI, but not with %FM or FMI. Effects of accelerated weight gain in early life on anthropometry and adiposity in adolescence varied in different growth windows. Accelerated weight gain during 6–18 months was associated with higher FM rather than linear growth. Effects of accelerated weight gain between 0 and 6 months varied with birth weight.