Serum Leptin Concentrations Research Articles

Maternal Serum and Cord Blood Leptin Concentrations in African Newborns: Relationship to Birth Weight and Gender

Background: Leptin, a protein predominantly produced by adipocytes, plays a crucial role in regulating energy balance, inflammation, immunity, and fetal growth. During pregnancy, maternal serum leptin levels increase, peaking in the second trimester, with placental production contributing to this rise. Leptin has also been identified in fetal tissues, and its concentration in umbilical cord blood correlates with birth weight. This study aimed to evaluate serum and umbilical cord blood leptin concentrations in rural Burundian women living in marginal nutritional conditions, and investigate potential gender differences in fetal leptin levels. Methods: We analyzed data from 38 healthy singleton pregnancies (20 male and 18 female newborns) delivered at Hôpital Autonome de Ngozi, Burundi. Leptin concentrations were measured in maternal and umbilical cord blood samples. Results: Our results revealed that neonatal leptin levels were significantly higher in female compared to male newborns, consistent with findings in other populations. Leptin concentrations in umbilical cord blood were positively correlated with neonatal birth weight and the Kaup index, while maternal leptin levels did not show such associations. Conclusions: Despite the challenging nutritional environment in this rural African setting, our findings suggest that leptin’s role in fetal growth regulation may transcend maternal nutritional status. The gender difference observed in leptin levels could be linked to genetic or epigenetic factors rather than fat content or reproductive hormones. This study supports the notion that leptin may be an important regulator of fetal development, even in malnourished populations, and underscores the need for further research to elucidate its mechanisms in pregnancy.

LCN2 blockade mitigating metabolic dysregulation and redefining appetite control in type 2 diabetes

LCN2 has an osteokine important for appetite regulation; in type 2 diabetes (T2D) it is not known whether appetite regulation mediated by LCN2 in the brain is altered. In this work, we focus on exploring the role of blocking LCN2 in metabolic health and appetite regulation within the central nervous system of mice with T2D. Material and methods: 4-week-old male C57BL/6 mice were used, divided into four experimental groups: intact, T2D, TD2/anti-LCN2, and T2D/IgG as isotype control. T2D was induced by low doses of streptozotocin and a high-carbohydrate diet. LCN2 blockade was performed by intraperitoneal administration of a polyclonal anti-LCN2 antibody. We analyzed metabolic parameters, food intake, feeding patterns, and serum LCN2 and leptin concentrations. In another group of intact or T2D mice, we analyzed the effect of blocking LCN2 and recombinant LCN2 on food consumption in a fasting-refeeding test and, the expression of cFOS and LCN2 in brain sections, specifically in the hypothalamus, piriform cortex, visceral area, arcuate nucleus and caudate-putamen. Results: T2D caused an increase in serum LCN2, without alterations in Ad libitum feeding, but with changes in the feeding pattern associated with alterations in LCN2-cFOS signalling in hypothalamic and non-hypothalamic brain regions. Blocking LCN2 improved metabolic parameters, increased Ad libitum feeding, and restored the feeding pattern after fasting, which is associated with enhanced LCN2 signalling in the brain. Conclusions: Blocking LCN2 restores metabolic health and normalizes the pattern of food consumption by normalizing LCN2 signalling in different brain regions.Graphical

Obese Hypertensive Men Have Fasting Serum Concentrations of Leptin Similar to Those of Obese Normotensive Men.

Leptin is a hormone which is secreted by the adipocytes. In the circulation, leptin levels are directly proportional to the body fat percentage. Studies have shown that higher leptin levels are associated with an increased risk of hypertension after adjusting for body mass index (BMI). Therefore, leptin has been proposed as a mediator of obesity-related hypertension. Whether leptin is associated with hypertension when controlling for body fat percentage remains unclear. We studied 103 obese men (BMI ≥30.0kg/m2). All men were healthy and were medication-free. We measured blood pressure using 24-hour ambulatory blood pressure (ABP) recordings. Hypertension was defined as 24-hour systolic ABP ≥130mm Hg and/or 24-hour diastolic ABP ≥80mm Hg, and normotension was defined as 24-hour ABP <130/80mm Hg. We measured fasting serum leptin concentrations and used dual-energy X-ray absorptiometry scanning to determine body fat percentage. Of the 103 obese men, 64 were hypertensive (24-hour systolic ABP (mean ± standard deviation) 137±11mg Hg and 24-hour diastolic ABP 83±6mm Hg) and 40 were normotensive (24-hour systolic ABP 117±6mg Hg and 24-hour diastolic ABP 73±4mm Hg). The 2 groups had similar fasting serum leptin concentrations (median (interquartile range)) 13.4 (5.7-36.1) µg/L versus 13.4 (5.4-27.1) µg/L, P=0.88) and total fat mass percentage (34.8±4.5% versus 34.0±4.7%, P=0.90). Obese hypertensive men have serum leptin concentrations similar to those of obese normotensive men with comparable body fat percentage measurements. This finding does not support leptin's candidacy as a mediator of obesity-related hypertension.

Диагностическая эффективность и прогностическая значимость антропометрических параметров как маркеров гиперлептинемии у подростков

Leptin is an energy homeostasis marker synthesized by cells of adipose tissue (adipocytes) and gastric mucosa. The search for clinical and anthropometric parameters associated with energy homeostasis disorders in excess body weight (BW) and obesity is necessary for stratification of patients at risk for early implementation of energy homeostasis disorders. The purpose of this re-search was to evaluate the relationship between serum leptin concentration and anthropometric parameters reflecting the topography of subcutaneous fat in adolescents of different ethnicities with excess BW and obesity in order to identify the most informative anthropometric parameters of energy homeosta-sis disorders. Materials and methods used: a single-center cross-sectional study of 362 adolescents aged 11 to 17 y/o residing in the Republic of Buryatia and the Irkutsk Oblast of Russia was conducted in 2015-2016 that included the participants as follows: 186 Caucasians (46 boys/140 girls) and 176 Mongoloids (96 boys/80 girls); 136 adolescents in the control group (38%) and 226 adolescents with excess BW and obesity (62%). All par-ticipants had their linear height, BW, waist (WC) and hip (HC) circumference, skinfold thickness measured as well as the body mass index (BMI, in kg per m2) calculated. The concentrations of glucose, total cholesterol, high-density, low-density and very low-density lipoprotein cholesterol, triglycerides and in-sulin were determined. The HOMA index was calculated. Serum leptin was de-termined by enzyme immunoassay using DBC Leptin ELISA kit (Diagnostics Biochem Canada Inc., Canada) with detection using BioTek Elx808 Microplate Spectrophotometer (Agilent Technologies, Inc., USA). Results: a strong posi-tive correlation was found between serum leptin levels and SDS BMI and trip-onderal BMI in adolescents of both ethnic groups: in Caucasian boys r=0.747 (p&lt;0.001), r=0.767 (p&lt;0.001), in Caucasian girls r=0.687 (p&lt;0.001) and r=0.695 (p&lt;0.001); in Mongoloid boys r=0.765 (p&lt;0.001), r=0.852 (p&lt;0.001), in Mongoloid girls r=0.612 (p&lt;0.001), r=0.667 (p&lt;0.001), respectively. Ac-cording to the results of ROC analysis, AUC WC/height showed good diagnos-tic significance for detecting hyperleptinemia (AUC=0.8-0.9) in adolescents from all the studied groups. Conclusion: the triponderal index and the WC/height ratio are informative anthropometric indicators for energy metabo-lism disorders and hyperleptinemia in Caucasian and Mongoloid adolescents of both genders with excess BW and obesity.

Gut microbiota are involved in leptin-induced thermoregulation in the Mongolian gerbil (Meriones unguiculatus).

Leptin is a hormone that is secreted by adipocytes and may promote energy expenditure by increasing thermogenesis. Our previous studies have shown that thermo-transient receptor potentials (thermo-TRPs) and gut microbiota are associated with thermoregulation in Mongolian gerbils, which are characterized by relative high serum leptin concentrations. Here, we tested whether leptin can stimulate non-shivering thermogenesis (NST) in Mongolian gerbils, and whether thermo-TRPs and gut microbiota are involved in leptin-induced thermogenesis. First, gerbils were given acute leptin treatment (ALT) with different doses. Results showed that ALT significantly increased the body temperature of gerbils and changed the composition of gut microbiota. Moreover, ALT groups showed a trend towards increased expression of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). Then, we investigated the effect of chronic leptin treatment (CLT) on gerbils. Surprisingly, CLT did not affect gerbils' food intake and body mass, but it significantly increased the body temperature at the end. Further, CLT did not affect the expression of thermogenic markers in BAT, white adipose tissue (WAT) or skeletal muscle. However, CLT increased the expression of leptin receptors and TRPV2 in the small intestine and affected the composition of gut microbiota. Together, our data suggest leptin may increase body temperature by regulating gut microbiota. In conclusion, serum hyperleptin in Mongolian gerbils is beneficial for adapting to cold environments, and TRPV2 and gut microbiota are involved.

Metabolic profile and adipokines in cardio-reno metabolic syndrome stages 1 and 2 in young people

Objective: to compare metabolic parameters and adipokine levels in cardiorenal metabolic syndrome (CRMS) stages 1 and 2 in young individuals aged 25–44 years.Materials and methods: a cross-sectional study based on a prospective cohort study included 120 people aged 25–44 years: group 1 (controls) — young individuals without cardiometabolic risk factors, stage 0 (n=40), group 2 — young individuals with CMS stage 1 (n=40), group 3 — young individuals with CMS stage 2 (n=40).Results: the most significant differences in the groups with stage 1 and 2 CRMS were observed for HOMA-IR index, glycosylated hemoglobin, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, triglycerides, and uric acid in comparison with the control group. The most common cardiometabolic risk factors in the group with stage 2 CRMS were overweight/obesity, hyperlipidemia, hyperglycemia, arterial hypertension, hyperuricemia, and a burdened heredity for cardiovascular diseases. The serum concentration of leptin was highest in women with stage 1 and 2 CRMS, whereas the serum concentration of adiponectin was lower in all individuals with stage 1 and 2 CRMS than in the control group, with no gender differences.Conclusion: modern approaches to the stages of CRMS contribute to the integration of cardiovascular diseases and metabolic disorders as components of a single pathophysiological process. They also allow a comprehensive and quantitative assessment of the likelihood of cardiovascular disease and type 2 diabetes mellitus. Measuring serum cytokine levels can serve as an effective tool for assessing overall cardiometabolic risk and predicting the development of cardiovascular diseases and type 2 diabetes mellitus.

New Insights into Health Conditions Related to Malfunctions in Clock Genes

Chronotypes play a crucial role in regulating sleep–wake cycles and overall health. The aim of this study was to investigate chronotype, sleep quality, polymorphisms of clock genes and the level of leptin in serum. We used standardized questionnaires to assess chronotype and sleep quality. Genetic analysis was performed to determine the selected clock gene polymorphism. Serum leptin level was measured by the Elisa method. The results showed that serum leptin concentration was elevated in women, as well as in men who had a high waist-to-hip ratio (WHR) and body mass index (BMI). The evidence indicated that younger students (&lt;22 years old) were most likely to experience poor sleep quality. Nevertheless, our multivariate analysis revealed that young age and a morning-oriented chronotype were associated with better sleep quality. We noted that clock gene polymorphisms were present in 28.6% of the participants. Moreover, polymorphisms of PER1 c.2247C&gt;T (rs2735611) and PER2 c.-12C&gt;G (rs2304672) genes were associated with serum leptin level and chronotype, respectively. These findings provide insights into the relationships between chronotype, sleep quality, clock gene polymorphisms and obesity risk in biomedical students. Understanding these factors can contribute to better sleep management and potential interventions to improve health outcomes in humans.

Methyl-donor supplementation in women with systemic lupus erythematosus with different nutritional status: the protocol for a randomised, double-blind, placebo-controlled trial

IntroductionDNA hypomethylation in patients with systemic lupus erythematosus (SLE) has been recently documented in the literature. Low levels of DNA methylation have been observed globally and in genes associated with...

PSIX-12 Influence of obesity on satiety hormones, serum metabolome, and fecal microbiome in adult dogs

Abstract The objective of this study was to investigate the difference between lean and obese dogs in terms of their satiety hormones, serum metabolome, and fecal microbiome. Mixed-breed lean (n = 30; 17 male and 13 female; 4.0 ± 2.5 yr of age; 24.6 ± 6.3% body fat) and obese (n = 30; 19 male and 11 female; 7.3 ± 2.1 yr of age; 46.9 ± 3.9% body fat) adult dogs were used in this study. Blood samples were collected to measure satiety hormones and serum metabolome, and fresh fecal samples were collected for microbiome analysis. It was hypothesized that obese dogs had altered metabolism and gut microbiome compared with lean dogs. Data were analyzed using MIXED procedure of SAS, using body type as the fixed effect and dog as the random effect. Results showed that obese dogs had greater (P &amp;lt; 0.05) serum leptin, insulin, and insulin-like growth factor-1 (IGF-1) concentrations, but reduced (P &amp;lt; 0.05) gastric inhibitory peptide (GIP) than lean dogs. Serum concentrations of all essential amino acids except for threonine in obese dogs were greater (P &amp;lt; 0.05) than in lean dogs. Obese dogs also had greater (P &amp;lt; 0.05) concentrations of serum N-Lactoyl amino acids and dipeptides except for prolylglycine than their lean counterparts. Additionally, concentrations of serum long-chain saturated and monounsaturated fatty acids were less (P &amp;lt; 0.05; only for myristate, pentadecanoate, and non-adecanoate) or similar in obese dogs compared with lean dogs. Serum oxidative stress makers, such as oxidized glutathione, cysteine-glutathione, and 4-hydroxynonenal, were greater (P &amp;lt; 0.05) in obese dogs than lean dogs. Furthermore, obese dogs had less (P &amp;lt; 0.05) fecal Firmicutes, but greater (P &amp;lt; 0.05) fecal Bacteroidetes and Fusobacteria, compared with lean dogs. There were no differences (P &amp;gt; 0.10) in fecal microbiome alpha diversity, such as Chao1 and Shannon index, between lean and obese dogs. In conclusion, obese dogs had differential body metabolism and gut microbiome compared with lean dogs.

Leptin signalling altered in infantile nephropathic cystinosis-related bone disorder.

The CTNS gene mutation causes infantile nephropathic cystinosis (INC). Patients with INC develop Fanconi syndrome and chronic kidney disease (CKD) with significant bone deformations. C57BL/6 Ctns-/- mice are an animal model for studying INC. Hyperleptinaemia results from the kidney's inability to eliminate the hormone leptin in CKD. Ctns-/- mice have elevated serum leptin concentrations. Leptin regulates bone metabolism through its receptor that signals further via the hypothalamic melanocortin 4 receptor (MC4R). Leptin signalling may affect bone health in Ctns-/- mice. We first defined the time course of bone abnormalities in Ctns-/- mice between 1 and 12months of age. We used both genetic and pharmacological approaches to investigate leptin signalling in Ctns-/- mice. We generated Ctns-/-Mc4r-/- double knockout mice. Bone phenotype of Ctns-/-Mc4r-/- mice, Ctns-/- mice and wild type (WT) mice at 1, 4, and 9months of age were compared. We then treated 12-month-old Ctns-/- mice and WT mice with a pegylated leptin receptor antagonist (PLA) (7mg/kg/day, IP), a MC4R antagonist agouti-related peptide (AgRP) (2nmol, intracranial infusion on days 0, 3, 6, 9, 12, 15, 18, 21, 24, and 27), or vehicle (normal saline), respectively, for 28days. Whole-body (BMC/BMD, bone area) and femoral bone phenotype (BMC/BMD, bone area, length and failure load) of mice were measured by DXA and femoral shaft biochemical test. We also measured lean mass content by EchoMRI and muscle function (grip strength and rotarod activity) in mice. Femur protein content of JAK2 and STAT3 was measured by ELISA kits, respectively. Bone defects are present in Ctns-/- mice throughout its first year of life. The deletion of the Mc4r gene attenuated bone disorder in Ctns-/- mice. Femoral BMD, bone area, length, and strength (failure load) were significantly increased in 9-month-old Ctns-/-Mc4r-/- mice than in age-matched Ctns-/- mice. PLA and AgRP treatment significantly increased femoral bone density (BMC/BMD) and mechanical strength in 12-month-old Ctns-/- mice. We adopted the pair-feeding approach for this study to show that the protective effects of PLA or AgRP on bone phenotype are independent of their potent orexigenic effect. Furthermore, an increase in lean mass and in vivo muscle function (grip strength and rotarod activity) are associated with improvements in bone phenotype (femoral BMC/BMD and mechanical strength) in Ctns-/- mice, suggesting a muscle-bone interplay. Decreased femur protein content of JAK2 and STAT3 was evident in Ctns-/- mice. PLA or AgRP treatment attenuated femur STAT3 content in Ctns-/- mice. Our findings suggest a significant role for dysregulated leptin signalling in INC-related bone disorder, either directly or potentially involving a muscle-bone interplay. Leptin signalling blockade may represent a novel approach to treating bone disease as well as muscle wasting in INC.

The influence of nutritional status, lipid profile, leptin concentration and polymorphism of genes encoding leptin and neuropeptide Y on the effectiveness of immunotherapy in advanced NSCLC patients

IntroductionNeuropeptide Y is a neurotransmitter in the nervous system and belongs to the orexigenic system that increases appetite. Its excessive secretion leads to obesity. Leptin is a pro-inflammatory adipokine (produced in adipose tissue) induced in obesity and may mediate increased antitumor immunity in obesity (including the promotion of M1 macrophages). Leptin and neuropeptide Y gene polymorphisms, causing increased leptin levels and the occurrence of obesity, and lipid profile disorders, may increase the effectiveness of immunotherapy.Materials and methodsIn 121 patients with advanced NSCLC without mutations in the EGFR gene and rearrangements of the ALK and ROS1 genes, undergoing immunotherapy (1st and 2nd line of treatment) or chemoimmunotherapy (1st line of treatment), we assessed BMI, lipid profile, PD-L1 expression on cancer cells using the immunohistochemical method (clone SP263 antibody), leptin concentration in blood serum by ELISA, polymorphisms in the promoter region of the genes for leptin (LEP) and neuropeptide Y (NPY) by real-time PCR.ResultsLeptin concentration was significantly higher in obese patients than in patients with normal or low weight (p = 0.00003) and in patients with disease stabilization compared to patients with progression observed during immunotherapy (p = 0.012). Disease control occurred significantly more often in patients with the GA or AA genotype than patients with the GG genotype in the rs779039 polymorphism of the LEP gene. The median PFS in the entire study group was five months (95% CI: 3-5.5), and the median OS was 12 months (95% CI: 8–16). Median PFS was highest in patients with TPS ≥ 50% (6.5 months) and in obese patients (6.6 months). Obese patients also had a slightly longer median OS compared to other patients (23.8 vs. 13 months). The multivariate Cox logistic regression test showed that the only factor reducing the risk of progression was TPS ≥ 50% (HR = 0.6068, 95% CI: 0.4001–0.9204, p = 0, 0187), and the only factor reducing the risk of death was high leptin concentration (HR = 0.6743, 95% CI: 0.4243–1.0715, p = 0.0953).ConclusionAssessment of nutritional status, serum leptin concentration and polymorphisms in the LEP gene may be of additional importance in predicting the effectiveness of immunotherapy and chemoimmunotherapy in patients with advanced NSCLC.

Leptin in reproduction and hypertension in pregnancy.

Leptin has important roles in numerous physiological functions, including those in the regulation of energy balance, and in immune and reproductive systems. However, in the recent years, evidence has implicated it in a number of obesity-related diseases, where its concentrations in serum are significantly elevated. Elevated serum leptin concentrations and increased placental leptin secretion have been reported in women with hypertensive disorders of pregnancy. Whether leptin is responsible for this disorder remains to be established. Leptin injections in healthy rats and mice during pregnancy result in endothelial activation, increased blood pressure and proteinuria. A potential role for leptin in the pathogenesis of pre-eclampsia is hypothesised, particularly in women who are overweight or obese where serum leptin concentrations are often elevated. This review summarises pertinent information in the literature on the role of leptin in puberty, pregnancy, and hypertensive disorders of pregnancy. In particular, the possible mechanism that may be involved in leptin-induced increase in blood pressure and proteinuria during pregnancy and the potential role of marinobufagenin in this disease entity. We hypothesise a significant role for oxidative stress in this, and propose a conceptual framework on the events that lead to endothelial activation, raised blood pressure and proteinuria following leptin administration.

A quantitative pipeline to assess secretion of human leptin coding variants reveals mechanisms underlying leptin deficiencies

The hormone leptin, primarily secreted by adipocytes, plays a crucial role in regulating whole-body energy homeostasis. Homozygous loss-of-function mutations in the leptin gene (LEP) cause hyperphagia and severe obesity, primarily through alterations in leptin's affinity for its receptor or changes in serum leptin concentrations. Although serum concentrations are influenced by various factors (e.g., gene expression, protein synthesis, stability in the serum), proper delivery of leptin from its site of synthesis in the endoplasmic reticulum via the secretory pathway to the extracellular serum is a critical step. However, the regulatory mechanisms and specific machinery involved in this trafficking route, particularly in the context of human LEP mutations, remain largely unexplored.We have employed the Retention Using Selective Hooks (RUSH) system to elucidate the secretory pathway of leptin. We have refined this system into a medium-throughput assay for examining the pathophysiology of a range of obesity-associated LEP variants. Our results reveal that leptin follows the default secretory pathway, with no additional regulatory steps identified prior to secretion.Through screening of leptin variants, we identified three mutations that lead to proteasomal degradation of leptin and one variant that significantly decreased leptin secretion, likely through aberrant disulfide bond formation. These observations have identified novel pathogenic effects of leptin variants, which can be informative for therapeutics and diagnostics. Finally, our novel quantitative screening platform can be adapted for other secreted proteins.

Total Gestational Weight Gain Is Explained by Leptin and Body Fat, Regardless of Pre-Pregnancy Body Mass Index and Other Adipokines, in Mexican Adolescents.

Pre-pregnancy body mass index (pBMI) is a predictor of gestational weight gain (GWG). However, other factors, such as adipokines and inflammation markers, may also be associated with GWG. The aim of the study was to determine the association of leptin, adiponectin, irisin, and C-reactive protein, with GWG in adolescents. A longitudinal study was conducted from 2018 to 2023 in adolescents with a clinically healthy pregnancy. The assessments included sociodemographic and clinical data, pBMI, percent of body fat, serum concentrations of leptin, adiponectin, irisin, and high-sensitivity C-reactive protein (hsCRP), and total GWG adequacy. Cox regression models were performed, the outcome variables were inadequate and excessive GWG. In 198 participants, being overweight/obesity was marginally associated with a protective effect against inadequate GWG (HR = 0.44, 95%CI = 0.18-1.06), regardless of maternal characteristics and adipokines. Leptin (HR = 1.014, 95%CI = 1.008-1.021), and body fat percent (HR = 1.11, 95%CI = 1.05-1.17) were associated with a higher risk of excessive GWG, independent of other maternal variables such as pBMI, while adiponectin was associated with a lower risk. These findings suggest that, in Mexican adolescents, adipose tissue and its adipokines during pregnancy may play a more significant role in the final GWG than body weight.

The effect of sucrose consumption on eating behavior and depression during morphine withdrawal period in rats

BACKGROUND: Sugary drink and junk food consumption increases during the withdrawal period, leading to subsequent psychological and metabolic alterations. OBJECTIVES: We aimed to investigate the relationship of sucrose consumption with serum insulin levels, leptin levels, brain Dopamine-2 receptor (D2R) expression, food consumption, and anxiety-depression findings in morphine-withdrawal rats. METHODS: Thirty-six male Wistar albino rats were divided into six groups: Control, sucrose-free, 5% sucrose, 10% sucrose, 20% sucrose, and an addiction test. Saline was intraperitoneally injected to the control group, and morphine was intraperitoneally injected to the other groups for 14 days. After 14 days, naloxone was administered to the addiction test group, and addiction symptoms were observed and this group was sacrificed on the same day. Other groups were fed ad libitum with different concentrations of sucrose solution for one week. Behavioral parameters were evaluated at the end of the experiment. Leptin and insulin concentrations in serum and D2R levels in brain tissues were detected using an enzyme-linked immunosorbent assay. D2R concentrations in brain tissues were evaluated utilizing immunohistochemistry. RESULTS: We observed decreased food consumption and increased fluid consumption in rats that consumed sucrose water during the withdrawal period. The level of depression and binge eating behavior was elevated in groups consuming sucrose, and the 10% sucrose group had the highest carbohydrate consumption and anxiety levels. In addition, the 10% sucrose group had the lowest brain D2R expression. The leptin level was highest in the 20% sucrose group. CONCLUSIONS: These results show the possible effects of sugary drinks consumed during the withdrawal period.

Serum insulin-like growth factor-1 and leptin concentrations in Black Bengal goats at different ages and gestation periods and their relationship to kid growth performance.

The impact of maternal hormone concentration on kid growth performance in relation to insulin-like growth factor 1 (IGF-1) and leptin is minimal. This study examined IGF-1 and leptin levels at varying ages and gestation periods for their correlation with Black Bengal goat kids' growth during the preweaning phase. Blood samples were collected from 43 dams with different reproductive cycles and 28 prepubertal goats to measure serum concentrations of IGF-1 and leptin. Among dams, both hormones were investigated in different age ranges (<2, 2-3, 3-4, and >4 years old) and reproductive cycles (non-pregnancy, early gestation (1-50 days), mid-gestation (51-100 days), late gestation (101-135 days), and the last 15 days before delivery). After delivery, 65 kids from 34 dams were weighted weekly for 8 weeks to calculate average daily weight gain (ADG) at 0-4 weeks (ADG0-4 W) and 4-8 weeks (ADG4-8 W) and growth performance, including weight (W), height (H), length (L), chest girth (C) measured at birth (W0, H0, L0, and C0) and at 10 weeks of age (W10, H10, L10, and C10) were related to hormone serum concentrations in their dams at different gestation periods including the last 15 days before delivery. Dams had higher mean serum IGF-1 (p < 0.001) and leptin (p < 0.05) than prepubertal goats. Dams at late gestation had higher IGF-1 concentrations than those at early and mid-gestation and during the last 15 days before delivery. However, it was consistent with non-pregnant goats. The kid's growth performance correlated positively with IGF-1 concentration, which was collected in the last 15 days before delivery. Multivariate analysis showed that ADG0-4 W was higher in kids born from dams with high IGF-1 than those with low IGF-1 measured during the last 15 days of delivery, whereas leptin tended to have a similar effect. Serum IGF-1 and leptin concentrations of dams measured during the last 15 days before delivery were associated with kid's growth during the preweaning period.

Diagnostic and Prognostic Value of Serum Leptin in Critically Ill Patients with Acute versus Acute-on-Chronic Liver Failure.

Differentiation between acute liver failure (ALF) and acute-on-chronic liver failure (ACLF) can be challenging in patients with de novo liver disease but is important to indicate the referral to a transplant center and urgency of organ allocation. Leptin, an adipocyte-derived cytokine that regulates energy storage and satiety, has multiple regulatory functions in the liver. We enrolled 160 critically ill patients with liver disease and 20 healthy individuals to measure serum leptin concentrations as a potential biomarker for diagnostic and prognostic purposes. Notably, patients with ALF had higher concentrations of serum leptin compared to patients with decompensated advanced chronic liver disease (dACLD) or ACLF (110 vs. 50 vs. 29 pg/mL, p < 0.001). Levels of serum leptin below 56 pg/mL excluded ALF in patients with acute hepatic disease, with a negative predictive value (NPV) of 98.8% in our cohort. Lastly, serum leptin did not show any dynamic changes within the first 48 h of ICU treatment, especially not in comparison with patients with ALF vs. ACLF or survivors vs. non-survivors. In conclusion, serum leptin may represent a helpful biomarker to exclude ALF in critically ill patients who present with acute liver dysfunction.

Functional Gastrointestinal Symptoms in Children with Autism and ADHD: Profiles of Hair and Salivary Cortisol, Serum Leptin Concentrations and Externalizing/Internalizing Problems.

Functional Gastrointestinal Disorders (FGIDs) present a higher prevalence in individuals with Neurodevelopmental Disorders (NDDs). The Stress System and the Gut-Brain axis (GBA) may mediate these relations. We aimed to assess the prevalence and profile of FGIDs in a clinical sample of children with Autism Spectrum Disorder (ASD) and Attention Deficit/Hyperactivity Disorder (ADHD) compared to typically developing children (TD) as well as to investigate possible relations between stress-related biomarkers and internalizing/externalizing problems in children with NDDS. In total, 120 children, aged between 4 and 12 years old, formed three groups (N = 40, each): ADHD, ASD and TD. Salivary cortisol, hair cortisol and serum leptin were measured. The ASD group had more FGID problems than the TD group (p = 0.001). The ADHD and ASD groups had higher total internalizing/externalizing problems than the TD group (p < 0.0001, p < 0.0001, p = 0.005, respectively). Children with FGIDs showed more total, internalizing and externalizing problems compared to children without FGIDs (p < 0.0001, p < 0.0001, p = 0.041, respectively). The ADHD group showed lower AUCg values (p < 0.0001), while the hair cortisol was higher for the TD group (p < 0.0001). In conclusion, children with NDDs had more FGID symptoms and present higher internalizing and externalizing problems. Children with ADHD and FGIDs had more internalizing problems compared to those without FGIDs. No differences in stress-related biomarkers were shown to differentiate children with NDDs with and without FGIDs. Future prospective studies including a greater number of children may elucidate the biological pathways linking these comorbidities.

The serum leptin can be a predictable marker for gestational diabetes mellitus

This study assessed the serum leptin concentrations for development of gestational diabetes mellitusThis is a case-control study, included 120 participants (60: Gestational Diabetes Mellitus Cases and 60: Healthy Controls). We assed BMI, FBS, HbA1c, Lipid Profile and serum leptin. The serum leptin concentrations were significantly elevated in patients with gestational diabetes mellitus when compared to controls (P=0.001**). There was a significant positive correlation between the serum leptin and BMI, FBS, HbA1c, Total Cholesterol and LDL (P=0.001**). Based on study findings, significant elevated levels of serum leptin might be served as a marker for detection of gestational diabetes mellitus.

Leptin attenuates the osteogenic induction potential of BMP9 by increasing β-catenin malonylation modification via Sirt5 down-regulation.

BMP9 has demonstrated significant osteogenic potential. In this study, we investigated the effect of Leptin on BMP9-induced osteogenic differentiation. Firstly, we found Leptin was decreased during BMP9-induced osteogenic differentiation and serum Leptin concentrations were increased in the ovariectomized (OVX) rats. Both in vitro and in vivo, exogenous expression of Leptin inhibited the process of osteogenic differentiation, whereas silencing Leptin enhanced. Exogenous Leptin could increase the malonylation of β-catenin. However, BMP9 could increase the level of Sirt5 and subsequently decrease the malonylation of β-catenin; the BMP9-induced osteogenic differentiation was inhibited by silencing Sirt5. These data suggested that Leptin can inhibit the BMP9-induced osteogenic differentiation, which may be mediated through reducing the activity of Wnt/β-catenin signalling via down-regulating Sirt5 to increase the malonylation level of β-catenin partly.