Serum Leptin Concentrations Research Articles

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

Leptin is a hormone that 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 test 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 change 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 weight, but it significantly increased the body temperature at the end. Besides, CLT did not affect the expression of thermogenic markers in BAT, white adipose tissue (WAT) and 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, the Mongolian gerbils with serum hyperleptin is beneficial for adapting the cold living environments, and TRPV2 and gut microbiota are involved.

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 (<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>T (rs2735611) and PER2 c.-12C>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 < 0.05) serum leptin, insulin, and insulin-like growth factor-1 (IGF-1) concentrations, but reduced (P < 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 < 0.05) than in lean dogs. Obese dogs also had greater (P < 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 < 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 < 0.05) in obese dogs than lean dogs. Furthermore, obese dogs had less (P < 0.05) fecal Firmicutes, but greater (P < 0.05) fecal Bacteroidetes and Fusobacteria, compared with lean dogs. There were no differences (P > 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.

Differential Acute Adipogenic Signaling Changes Following Neuromusculoskeletal Injuries

Following traumatic injury, neuromusculoskeletal tissue undergoes extensive plastic modification. Changes can be observed at the local and systemic levels and can involve tissue function, signaling, and local composition. Currently there is limited understanding of early adipogenic changes following some traumatic injuries, which is needed to understand the long-term lack of functional muscle recovery. The objective of this project was to examine plasticity after injury, namely systemic and local adipogenic signaling and fat droplet deposition following volumetric muscle loss (VML) and denervation injuries. We hypothesized there would be differential changes in local and systemic adipogenic signaling, specifically changes in fat droplet accumulation following neuromusculoskeletal injuries. Adult C57B1/6J mice (n=36; 6 male, 6 female/group): posterior compartment VML, tibial nerve denervation, and naïve control. Both injury models target plantarflexor muscles. Mice were euthanized 72-hrs post-injury. In vivo muscle function was assessed, and gastrocnemius, liver, and serum were saved for analysis. Whole gastrocnemius muscles from a subset (n=4/group) were saved for histology, and five standardized sections were systematically obtained 1.5mm apart; muscle sections were stained with H&amp;E and Oil-Red-O to evaluate total fiber number and fat droplet accumulation, respectively. Data were analyzed by two- and three-way ANOVA with Tukey’s HSD post hoc. Maximal torque declined ~81 and 98% following VML and denervation injury, respectively (main effect p&lt;0.001), and VML-injured muscle was more fatigable than injury naïve (main effect p=0.001). Following denervation, liver insulin-like growth factor 1 (IGF-1) was increased ~52% compared to other groups, and was most pronounced in males (main effect injury p&lt;0.001; sex p=0.021). VML injury resulted in a 4-fold higher muscle IGF-1 regardless of sex (interaction p=0.021), and greater muscle interleukin-6 (IL-6), which was more pronounced in females (main effect injury p=0.001; sex p=0.049). Platelet-derived factor growth receptor (PDFGRα) expression was diminished following VML injury in both sexes (interaction p=0.016); suggesting a decrease in fibro-adipogenic progenitors (FAPs) and an alternative origin responsible for increases in IGF-1 and IL-6 rather than FAPs. Serum leptin concentrations were blunted following both VML- and denervation-injury (main effect p=0.002), which may illicit alterations in the regenerative process, specifically the maintenance of muscle quality. Serum IGF-1 and IL-6 concentrations were not affected by injury (p≥0.164). Histological analysis revealed a significant decrease in total fiber number across the middle three sections of the VML-injured muscle (i.e., the section initially injured) compared to other groups (p≤0.034). Findings provide a foundation for characterizing adipocyte development in the muscle remaining after injury and identify therapeutic targets for rehabilitative and nutritional approaches to address contractile and metabolic impairments following injury. Future work should elucidate the time course of adipogenic signaling following these injuries, with particular interest in their relationship to changes in metabolic and contractile impairments. R01-AR078903 (JAC &amp; SMG); University of Minnesota UROP (BAC). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Effect of Maternal Overweight/Obesity on Serum and Breastmilk Leptin, and Its Associations with Body Composition, Cardiometabolic Health Indices, and Maternal Diet: The BLOOM Study.

In overweight and obese patients, elevated serum and breastmilk leptin concentrations are observed, with serum leptin also being likely affected by the diet. We analyzed serum and breastmilk leptin in normal weight (NW) and overweight/obese (OW/OB) mothers, and evaluated its associations with (1) maternal anthropometric parameters; (2) markers of cardiometabolic health; and (3) the maternal diet. The BLOOM (Breastmilk and the Link to Overweight/Obesity and Maternal diet) study was conducted among 40 women (n = 20 OW/OB; n = 20, NW) who were exclusively or predominantly breastfeeding for 15.5 ± 1.2 (OW/OB group (0.99)) weeks. We collected 24 h breastmilk and fasting blood samples for leptin analysis by ELISA. Maternal dietary habits were evaluated using a 3-day dietary record and food frequency questionnaire, which were used to calculate the Polish-adapted Mediterranean Diet score. Maternal anthropometric measurements and DEXA scans were performed, and anthropometric and cardiometabolic indices were calculated. The OW mothers had 1.4 times higher serum levels, while OB mothers had 4.5 and 6.2 higher serum and breastmilk leptin levels, respectively, in comparison to the NW mothers. The FM% was correlated with serum and breastmilk leptin levels (r = 0.878, r = 0.638). Serum leptin was associated with markers of cardiometabolic health such as AIP, CMI, and VAI in the NW mothers, and with LAP in the OW/OB mothers. Higher energy, fructose intake and adherence to the Mediterranean diet were associated with serum leptin in the NW mothers (β = 0.323, 0.039-0.608; β = 0.318, 0.065-0.572; β = 0.279, 0.031-0.528); meanwhile, higher adherence to the Mediterranean diet could protect against elevated breastmilk leptin concentrations in OW/OB mothers (β = -0.444, -0.839--0.050), even after adjustment for FM%. Our results suggest a potential association between maternal serum leptin concentrations and cardiometabolic health. In addition, we confirm the importance of healthy dietary patterns in the improvement of breastmilk composition.

Performance, HSP70 expression, antioxidant enzymes, oxidative DNA damage biomarkers, metabolic hormones, and intestinal microbiota of broiler chickens fed mistletoe leaf powder supplemented diets under tropical high ambient temperatures

The study investigated the impact of Mistletoe Leaf Powder (MLP) supplementation on some parameters in heat-stressed broiler chickens. The standard baseline diets, comprising four different formulations, were provided during the starter and finisher stages. Chickens were randomly assigned to the 4 dietary groups: a negative control (CON) with no supplementation, a positive control (VTC) with 200 mg/kg vitamin C, and 2 experimental treatment groups with 2500 mg/kg (MLP2) and 5000 mg/kg (MLP5) MLP supplementation. The Body Weight Gain (BWG) in MLP2 and MLP5 treatment groups was comparable (P > 0.05) to those in VTC, while the CON group exhibited significantly (P < 0.05) lower BWG. Feed consumption was significantly (P < 0.05) lower broiler chickens in the CON group compared to those VTC, MLP2, and MLP5. Heat shock protein 70 (HSP70) levels were lower in broiler chickens belonging to VTC, MLP2, and MLP5 groups compared to those in CON, and MLP2 showed no difference (P > 0.05) from MLP5 and VTC. Serum glutathione peroxidase and catalase concentrations were higher (P < 0.05) in birds belonging to MLP5, MLP2, and VTC groups compared to CON. The 8-hydroxy-2′-deoxyguanosine concentration was lower (P < 0.05) in birds of VTC, MLP2, and MLP5 compared to the CON, with VTC showing the least concentration. Serum insulin levels were higher (P < 0.05) in MLP5 compared to those in CON, while serum triiodothyronine and leptin concentrations were lower (P < 0.05) in CON compared to birds in VTC, MLP2, and MLP5. Microbiota analysis revealed that the Coliform bacteria population was higher (P < 0.05) in birds belonging to CON compared to those in VTC, MLP2, and MLP5 groups, whereas lactic acid-producing bacteria were significantly (P < 0.05) lower in birds of CON and highest in MLP2 and MLP5 groups. In conclusion, dietary supplementation of MLP at 5000 mg/kg enhanced performance, oxidative status, influenced metabolic hormones, and gut microbiota in broiler chickens raised under high ambient temperature.

Postnatal Consumption of Black Bean Powder Protects against Obesity and Dyslipidemia in Male Adult Rat Offspring from Obese Pregnancies.

The adverse influence of maternal obesity on offspring metabolic health throughout the life-course is a significant public health challenge with few effective interventions. We examined if black bean powder (BBP) supplementation to a high-calorie maternal pregnancy diet or a postnatal offspring diet could offer protection against the metabolic programming of metabolic disease risk in adult offspring. Female Sprague Dawley rats were randomly assigned to one of three diets (n = 10/group) for a 3-week pre-pregnancy period and throughout gestation and lactation: (i) a low-caloric control diet (CON); (ii) a high-caloric obesity-inducing diet (HC); or (iii) the HC diet with 20% black bean powder (HC-BBP). At weaning [postnatal day (PND) 21], one male pup from each dam was weaned onto the CON diet throughout the postnatal period until adulthood (PND120). In addition, a second male from the HC group only was weaned onto the CON diet supplemented with BBP (CON-BBP). Thus, based on the maternal diet exposure and offspring postnatal diet, four experimental adult offspring groups were compared: CON/CON, HC/CON, HC-BPP/CON, and HC/CON-BBP. On PND120, blood was collected for biochemical analysis (e.g., lipids, glycemic control endpoints, etc.), and livers were excised for lipid analysis (triglycerides [TG] and cholesterol) and the mRNA/protein expression of lipid-regulatory targets. Compared with the CON/CON group, adult offspring from the HC/CON group exhibited a higher (p < 0.05) body weight (BW) (682.88 ± 10.67 vs. 628.02 ± 16.61 g) and hepatic TG (29.55 ± 1.31 vs. 22.86 ± 1.85 mmol/g). Although maternal BBP supplementation (HC-BBP/CON) had little influence on metabolic outcomes, the consumption of BBP in the postnatal period (HC/CON-BBP) lowered hepatic TG and cholesterol compared with the other treatment groups. Reduced hepatic TG in the HC/CON-BBP was likely associated with lower postnatal BW gain (vs. HC/CON), lower mRNA and protein expression of hepatic Fasn (vs. HC/CON), and lower serum leptin concentration (vs. CON/CON and HC groups). Our results suggest that the postnatal consumption of a black-bean-powder-supplemented diet may protect male rat offspring against the programming of obesity and dyslipidemia associated with maternal obesity. Future work should investigate the bioactive fraction of BBP responsible for the observed effect.

Association between Toxoplasma gondii and gestational diabetes with regard to serum leptin and tumor necrosis factor alpha, a preliminary study

Gestational diabetes (GDM), the onset of any degree of glucose intolerance during pregnancy, increases a wide range of adverse health outcomes for both the mother and the fetus. The aim of the present study was to evaluate the association of Toxoplasma gondii infection with GDM in a case-control study with regard to the levels of leptin and tumor necrosis factor alpha (TNF-α) as two inflammatory biomarkers. Fifty-one pregnant diabetic cases and 109 controls were selected from a prenatal care clinic of a general hospital in Shiraz, southern Iran during July–November 2020. Cases and controls were similar in age, gestational age and number of parturitions. The presence of IgG antibodies against T. gondii, and serum concentrations of leptin and TNF-α were determined by ELISA. Anti-Toxoplasma antibodies were detected in 25 subjects (15.6 %, 95 % CI: 9.9–21.3). Nine (18 %) diabetic cases were infected with Toxoplasma compared to 16 (15 %) healthy controls (P = 0.63). Level of leptin was higher (P = 0.07) while TNF-α was lower in diabetic cases compared to healthy controls (P = 0.08). When subjects were classified according to the combination of GDM and T. gondii, leptin was significantly lower in healthy (non-diabetic, non-infected) subjects compared to diabetics (P = 0.026), and TNF-α was higher in healthy subjects compared to Toxoplasma-infected diabetics (P = 0.032). These findings can be interpreted as both comorbidities being individually associated with increasing serum leptin and decreasing TNF-α concentrations, with modifying effects on each other. The present study opens a new perspective on GDM and its complex pathophysiological mechanism. Future research in this area is needed to better understand the underlying pathway for the development of GDM and the role of T. gondii and inflammatory biomarkers.