Hormone Leptin Research Articles

Ameliorative effects of Orlistat and metformin either alone or in combination on liver functions, structure, immunoreactivity and antioxidant enzymes in experimentally induced obesity in male rats

BackgroundPrevalence of obesity is increasing worldwide. Obesity is associated with incidences of metabolic disorders and cardiovascular diseases and the risk of having it rose sharply during the COVID-19 pandemic. Obesity is associated with oxidative stress, inflammatory markers and hepatic disorders and has become one of the silent killer diseases affecting global health. MethodsThis study examined the effects of obesity on liver functions (ALT, AST and LDH), lipid profile (TG, TC, HDL-c, LDL-c and vLDL-c), tumour necrosis factor alpha (TNF-α), inflammatory marker, C-reactive protein (CRP), leptin hormone and antioxidant enzymes (CAT, SOD and GPx) and lipid peroxidation marker (MDA) in liver homogenates besides histological structure of the liver tissues and assessment of DNA damage. Fifty male Wistar rats were used and they were divided into five treatment groups: I-Control group, II-high-fat diet (HFD) treated group (Obesity) group, III-HFD plus Orlistat (ORL), IV-HFD plus metformin (Met) and V- HFD plus ORL plus Met. ResultsExperimentally-induced obesity caused a significant increase in liver enzymes including lipid markers (triglycerides and total cholesterol), inflammatory markers, tumour markers and lipid peroxidation markers and a concurrent decline in antioxidant enzymes and damage of liver main structures characterised by presence of congestion and accumulation of mononuclear inflammatory cells in blood sinusoids. In contrast, groups treated with either ORL or Met or both group, we recorded restoration of normal hepatic structures and a decline in DNA damage, liver enzymes and antioxidant levels. The best restoration and amelioration were observed in the group treated with a combination of ORL and Met. ConclusionOur findings indicated the synergistic effect of ORL and Met in ameliorating hepatic functions and lipid profile, alleviating inflammation, genotoxicity and side effects of experimentally-induced obesity.

Association between LEPR Genotype and Gut Microbiome in Healthy Non-Obese Korean Adults.

The LEPR (leptin receptor) genotype is associated with obesity. Gut microbiome composition differs between obese and non-obese adults. However, the impact of LEPR genotype on gut microbiome composition in humans has not yet been studied. In this study, the association between LEPR single nucleotide polymorphism (rs1173100, rs1137101, and rs790419) and the gut microbiome composition in 65 non-obese Korean adults was investigated. Leptin, triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels were also measured in all participants. Mean ± SD (standard deviation) of age, body mass index, and leptin hormone levels of participants was 35.2 ± 8.1 years, 21.4 ± 1.8 kg/m2, and 7989.1 ± 6687.4 pg/mL, respectively. Gut microbiome analysis was performed at the phylum level by 16S rRNA sequencing. Among the 11 phyla detected, only one showed significantly different relative abundances between LEPR genotypes. The relative abundance of Candidatus Saccharibacteria was higher in the G/A genotype group than in the G/G genotype group for the rs1137101 single nucleotide polymorphism (p=0.0322). Participant characteristics, including body mass index, leptin levels, and other lipid levels, were similar between the rs1137101 G/G and G/A genotypes. In addition, the relative abundances of Fusobacteria and Tenericutes showed significant positive relationship with plasma leptin concentrations (p=0.0036 and p=0.0000, respectively). In conclusion, LEPR genotype and gut microbiome may be associated even in normal-weight Korean adults. However, further studies with a greater number of obese adults are needed to confirm whether LEPR genotype is related to gut microbiome composition.

An evaluation of basal metabolic rate among healthy individuals — a cross-sectional study

BackgroundThe main source of daily energy requirement in Asian societies is basal metabolic rate (BMR). Even though the reason for this fluctuation is debatable, prior research have shown that BMR is highly varied in individuals. All studies concur that variation in fat-free mass (FFM) is important, although the effects of fat mass (FM), age, sex, and the hormones leptin, triiodothyronine (T3), and thyroxine (T4) are still unknown.ObjectiveThe main objectives of the study are as follows:• To evaluate the basal metabolic rate among healthy individuals• To identify the risk factors on basal metabolic rate among healthy individualsMethodologyIn total, 50 individuals were consecutively enrolled in the study during the entrepreneurship studio on 29th June 2022 held at Garden City University (GCU). The inclusion criteria were age between 18 and 50 years, both males and females, students and professors of GCU, and healthy individuals. The exclusion criteria were subjects who had overt metabolic and/or endocrine diseases (e.g., diabetes, hypothyroidism, hypertension, amenorrhea) and those taking any drug known to influence energy metabolism. The convenient samples of 50 subjects were taken from this study.Outcome measuresBasal metabolic rate (BMR) and body mass index (BMI).ResultsThe demographic data, height, weight, BMI, and BMR were recorded. The mean and standard deviation of age are 25.81 ± 8.71 and 23.95 ± 6.67 of males and females, respectively. The mean and standard deviation of height are 1.68 ± 0.68 and 1.63 ± 0.07, respectively. The mean and standard deviation for weight are 63.8 ± 11.49 and 54.86 ± 10.43, respectively. The mean and standard deviation of BMI are males and females which are 22.3 ± 3.22 and 20.47 ± 3.62, respectively. The mean and standard deviation of BMR are males and females which are 1552.41 ± 127.3 and 1327.7 ± 147.9.ConclusionThe energy used up while lying still at rest and being awake during the nocturnal postabsorptive state is known as the basal metabolic rate (BMR). The values can be used as a reference for comparison with the normative values, and cardiorespiratory endurance training can be included in the rehabilitation program.

Neuronal Ptpn1 and Socs3 deletion improves metabolism but not anovulation in a mouse PCOS model.

Polycystic ovary syndrome (PCOS) is one of the most common causes of infertility in women. Approximately half of diagnosed individuals also experience metabolic syndrome. Central and peripheral resistance to the hormones insulin and leptin have been reported to contribute to both metabolic and reproductive dysregulation. In PCOS and preclinical PCOS animal models, circulating insulin and leptin levels are often increased in parallel with the development of hormone resistance, however it remains uncertain whether these changes contribute to the PCOS state. In this study we tested whether central actions of protein tyrosine phosphatase 1B (PTP1B) and suppressor of cytokine signaling 3 (SOCS3), negative regulators of insulin and leptin signaling pathways respectively, play a role in the development of PCOS-like phenotype. A peripubertal dihydrotestosterone (DHT) excess PCOS-like mouse model was used, which exhibits both metabolic and reproductive dysfunction. Mice with knockout of the genes encoding PTP1B and SOCS3 from forebrain neurons were generated, and metabolic and reproductive function were compared between knockout and control groups. DHT treatment induced mild insulin resistance but not leptin resistance, so the role of SOCS3 could not be tested. As expected, DHT excess abolished estrous cycles and corpora lutea presence and caused increased visceral adiposity and fasting glucose levels. Knockout mice did not show any rescue of reproductive dysfunction, but did have reduced adiposity compared to control DHT mice. These data suggest that negative regulation of central insulin signaling by PTP1B is not responsible for peripubertal DHT excess-induced reproductive impairments, but may mediate its increased adiposity effects.

An unusual signal transducer GIV/Girdin engages in the roles of adipocyte-derived hormone leptin in liver fibrosis

Obese patients usually have hyperleptinemia and are prone to develop liver fibrosis. Leptin is intimately linked to liver fibrogenesis, a multi-receptor-driven disease. Gα-Interacting Vesicle-associated protein (GIV) functions as a multimodular signal transducer and a guanine nucleotide exchange factor for Gi controling key signalings downstream of diverse receptors. This study aimed to examine the roles of GIV in leptin-caused liver fibrosis and employed the culture-activated hepatic stellate cells (HSCs) and leptin-deficient mice, respectively. Results indicated that leptin upregulated GIV expression in HSCs. GIV was involved in leptin-induced HSC activation and liver fibrosis. GIV mediated leptin regulation of TIMP1, MMP9, PDGFβ receptor and TGFβ receptor and was required for leptin stimulating the pathways of Erk1/2, Akt1, and Smad3. GIV was also a mediator for leptin-regulation of Cyclin D1 and Caspase-3 activity but GIV reduced Caspase-3 level independently of leptin in vivo. Erk1/2 signaling, Egr1 and c-Jun were associated with the effect of leptin on GIV expression in HSCs. Leptin-induced Erk1/2 signaling increased Egr1 and p-c-Jun levels and promoted their binding to GIV promoter at the sites between −190 bp and −180 bp and between −382 bp and − 376 bp, respectively. Egr1 knockdown lessened leptin-upregulation of GIV in vitro and in vivo. In human cirrhotic livers, the increase in GIV protein level parallelled with the elevated p-Erk1/2 and Egr1 levels in HSCs. In summary, the unusual signal transducer GIV was identified as an important mediator in leptin-induced liver fibrosis. GIV may have significant implications in liver fibrosis progression of obese patients with hyperleptinaemia.

The potential effect of leptin co-administration on photodynamic damage using quail chorioallantoic membrane model

BackgroundThe chorioallantoic membrane (CAM) of the Japanese quail is an excellent model for studying photodynamic therapy (PDT) due to its rich vascularization. PDT is used not only in oncological treatment but also in infectious diseases, or psoriasis, where it yields significant advantages. This treatment also has its limitations, such as burning, itching, erythema, redness, swelling, and delayed wound healing. The aim of this study was to analyse the potentially protective properties of the tissue hormone leptin during PDT. MethodsJapanese quail embryos incubated ex ovo were used in this experiment. On the 9th day of embryonic development, leptin (5 μg) and photosensitiser hypericin (79 μM) were topically applied, followed by irradiation. The effect of leptin co-administration was evaluated from CAM images and histological structure analysis, histological samples, and qPCR, where the expression of genes involved in angiogenesis, apoptosis, and oxidative stress was monitored. ResultsWe observed vascular damage in all experimental groups, the highest damage was found after the application of hypericin without leptin coadministration. Histological analysis confirmed the protective effect of leptin. qPCR analysis presented differences in FREK gene expression, but also in genes involved in oxidative stress like SOD, NRF-1, NRF-2, and GPX7. The application of leptin significantly reduced the expression of apoptosis regulatory proteins CASP3, cytochrome C, and APAF1. ConclusionsOur results in the CAM model suggest a possible protective effect of leptin to prevent PDT damage and aid in the subsequent regeneration of target tissues after antimicrobial PDT.

Elevated serum leptin is associated with attenuated reward anticipation in major depressive disorder independent of peripheral C-reactive protein levels

Major depressive disorder (MDD) is associated with immunologic and metabolic alterations linked to central processing dysfunctions, including attenuated reward processing. This study investigated the associations between inflammation, metabolic hormones (leptin, insulin, adiponectin), and reward-related brain processing in MDD patients with high (MDD-High) and low (MDD-Low) C-reactive protein (CRP) levels compared to healthy comparison subjects (HC). Participants completed a blood draw and a monetary incentive delay task during functional magnetic resonance imaging. Although groups did not differ in insulin or adiponectin concentrations, both MDD-High (Wilcoxon p = 0.004, d = 0.65) and MDD-Low (Wilcoxon p = 0.046, d = 0.53) showed higher leptin concentrations than HC but did not differ from each other. Across MDD participants, higher leptin levels were associated with lower brain activation during reward anticipation in the left insula (r = − 0.30, p = 0.004) and left dorsolateral putamen (r = -− 0.24, p = 0.025). In contrast, within HC, higher leptin concentrations were associated with higher activation during reward anticipation in the same regions (insula: r = 0.40, p = 0.007; putamen: r = 0.37, p = 0.014). Depression may be characterized by elevated pro-inflammatory signaling via leptin concentrations through alternate inflammatory pathways distinct to CRP.

Monitoring of leptin hormone levels in child bearing – age women in Baghdad / Iraq – with polycystic ovary syndrome, and the impact of BMI on leptin levels

Monitoring of leptin hormone levels in child bearing – age women in Baghdad / Iraq – with polycystic ovary syndrome, and the impact of BMI on leptin levels

Hubungan Kebiasaan Konsumsi Kopi dan Kualitas Tidur dengan Status Gizi pada Remaja di Kelurahan Jagakarsa Jakarta Selatan

The body has the hormones leptin and ghrelin that regulate appetite. An imbalance of these two hormones can result in changes in metabolism.. Currently, most adolescents consume excessive coffee which can cause metabolic disorders such as obesity. The purpose of this study was to analyze the relationship between coffee consumption and sleep quality with nutritional status in adolescents in Jagakarsa Village, South Jakarta. This research design uses cross sectional. Data collection using questionnaires by interviewed that have been tested for validity and anthropometric measurements of height and weight. The subjects in this study amounted to 95 people. Conducted in May - June 2022 Analysis of the relationship between coffee consumption variables and sleep quality with nutritional status using Chi-Square statistical test analysis. The results showed that most of the adolescents had normal nutritional status, namely 48 respondents. Coffee consumption habits based on frequency were mostly in the 1x / day category as many as 74 respondents, and based on quantity most were in the 1-2 cup / day category as many as 90 respondents. Sleep quality in the good category was 23 respondents and the bad category was 72 respondents. This study shows that there is no relationship between coffee consumption and nutritional status based on frequency (p=0.107), based on quantity of coffee consumption (p=0.090) and there is no relationship between sleep quality and nutritional status (p=0.116) in adolescents in Jagakarsa Village, South Jakarta. The conclusion of this study is that there is no significant relationship between coffee consumption variables and nutritional status. There is no significant relationship between sleep quality variables and nutritional status among adolescents in Jagakarsa Village, South Jakarta

Effects of flaxseed (Linum usitatissimum) on climacteric symptoms and clinical parameters in post-menopausal women

Menopause is the irreversible and permanent cessation of menstruation after one year of amenorrhea. Common symptoms include vaginal dryness, hot flashes, night sweating, and bone pain. Traditionally Linum usitatissimum (Flaxseeds) has been used for the treatment of postmenopausal symptoms. However, the effect of this medicinal herb on the satiety hormone; leptin and body weight in menopausal women has not been elucidated well. This study was designed to evaluate the effect of flaxseeds on serum estrogen, progesterone, leptin, and malondialdehyde, body mass index, blood pressure in menopausal women. Moreover, the flaxseed effect on climacteric symptoms was also investigated.
 The study was carried out as an interventional pre-post design. The study was a six-week oral administration of 1000 mg flaxseed powder twice daily by menopausal women. The duration of the study was eight months. Serum levels of estrogen, progesterone, and leptin hormones as well as total plasma malondialdehyde were determined pre-and-post flaxseed intervention. Clinical symptoms and bothersome complaints of postmenopausal women such as hot flashes, vaginal dryness, bone pain, and night sweating were also evaluated. Furthermore, blood pressure elements and body mass index were also measured. The results showed that Linum usitatissimum seed powder significantly reduced vaginal dryness, hot flashes, bone pain, and night sweating in menopausal women. The same dose of flaxseed had no significant effects on serum estrogen and progesterone. However, it significantly decreased serum malondialdehyde and increased serum leptin. Flaxseed had a non-significant effect on body mass index and blood pressure. In conclusion Linum usitatissimum seed had significant efficacy in relieving vasomotor symptoms, decreasing oxidative stress, and increasing serum levels of leptin in menopausal women.
 Keywords: climacteric, estrogen, progesterone, leptin, malondialdehyde.

Histaminergic regulation of food intake.

Histamine is a biogenic amine that acts as a neuromodulator within the brain. In the hypothalamus, histaminergic signaling contributes to the regulation of numerous physiological and homeostatic processes, including the regulation of energy balance. Histaminergic neurons project extensively throughout the hypothalamus and two histamine receptors (H1R, H3R) are strongly expressed in key hypothalamic nuclei known to regulate energy homeostasis, including the paraventricular (PVH), ventromedial (VMH), dorsomedial (DMH), and arcuate (ARC) nuclei. The activation of different histamine receptors is associated with differential effects on neuronal activity, mediated by their different G protein-coupling. Consequently, activation of H1R has opposing effects on food intake to that of H3R: H1R activation suppresses food intake, while H3R activation mediates an orexigenic response. The central histaminergic system has been implicated in atypical antipsychotic-induced weight gain and has been proposed as a potential therapeutic target for the treatment of obesity. It has also been demonstrated to interact with other major regulators of energy homeostasis, including the central melanocortin system and the adipose-derived hormone leptin. However, the exact mechanisms by which the histaminergic system contributes to the modification of these satiety signals remain underexplored. The present review focuses on recent advances in our understanding of the central histaminergic system's role in regulating feeding and highlights unanswered questions remaining in our knowledge of the functionality of this system.

Leptin, but not Estradiol, Signaling in PACAP Neurons Modulates Puberty Onset

Abstract The adipose-derived hormone leptin critically modulates reproductive function, such that its absence results in hypothalamic hypogonadism. Pituitary adenylate cyclase-activating polypeptide (PACAP)-expressing neurons are potential mediators of leptin's action on the neuroendocrine reproductive axis because they are leptin-sensitive and involved in both feeding behavior and reproductive function. In the complete absence of PACAP, male and female mice exhibit metabolic and reproductive abnormalities, yet there is some sexual dimorphism in the reproductive impairments. We tested whether PACAP neurons play a critical and/or sufficient role in mediating leptin's effects on reproductive function by generating PACAP-specific leptin receptor (LepR) knockout and rescue mice, respectively. We also generated PACAP-specific estrogen receptor alpha knockout mice to determine whether estradiol-dependent regulation of PACAP was critically involved in the control of reproductive function and whether it contributed to the sexually dimorphic effects of PACAP. We showed that LepR signaling in PACAP neurons is critically involved in the timing of female, but not male, puberty onset, but not fertility. Rescuing LepR-PACAP signaling in otherwise LepR-deficient mice was unable to rescue the reproductive deficits observed in LepR null mice but led to a marginal improvement in body weight and adiposity in females. Finally, PACAP-specific estrogen receptor alpha knockout did not lead to any changes in body weight or puberty onset compared with control mice. These data highlight that PACAP is a critical mediator of some of leptin's, but not estradiol's, influence on puberty onset in females, but is not critically involved in relaying leptin's effects in males or in adult females.

Developing a Beta Cell Vaccine in the Pancreatic Beta Cell Restoring Therapy for Treating Type First Diabetes

Gene transfer and biotechnology can develop new beta cells in the human body. Regenerative mechanisms under physiological and pathological conditions, factors involved in stimulation of regeneration, and potential pharmaceutical drugs are discussed. Replication is mediated by mitogenic signaling pathways and upstream activators. These mechanisms also involve upstream activators of mitogenic signaling pathways, including nutrients (glucose, calcium), epidermal and platelet-derived GFs (Glp1, Gip), and hormones (leptin, estrogen, prolactin, and progesterone).

Kidney bean protein hydrolysate as a fish meal replacer: Effects on growth, digestive enzymes, metabolic functions, immune-antioxidant parameters and their related gene expression, intestinal and muscular gene expression

A feeding trial for 70 days was designated on Nile tilapia, Oreochromis niloticus (O. niloticus). A total of 200 fish (34.38 ± 0.05 g) were assigned into five groups, four replicates for each (10 fish/replicate; 40 fish/group) and received five isonitrogenous and isocaloric diets with five replacement levels of fishmeal (FM) with kidney bean (Phaseolus vulgaris L) protein hydrolysate (KBH) (0, 25, 50, 75, 100%). The findings demonstrated a significant increase in the performance metrics (final body weight, total weight gain, average daily weight gain, protein efficiency ratio, and specific growth rate) with a considerable improvement in the feed conversion ratio across all replacement levels, with the greatest value obtained in the KBH75 and KBH100 groups. Regarding the broken line regression analysis, the optimum FM replacement level with KBH was 76%. By replacing FM with KBH, the growth hormone and digestive enzymes (amylase and protease) levels were significantly increased, whilst the glucose and leptin hormone levels significantly declined. The amino acid transporters (solute carrier family 15 member 2 and solute carrier family 26 member 6), insulin growth factor-1, the immune-associated genes (interleukin-8, toll-like receptors-7, and cc-chemokine), and the antioxidant-associated genes (glutathione peroxidase, superoxide dismutase, and Glutathione synthetase) expression was substantially boosted in all replacement levels, where the KBH50 group recorded the highest expression. As well as the mRNA expression of myostatin was down-turned in all replacement levels relative to the KBH0 group. Improving the immune functions (lysozyme, complement 3, nitric oxide, phagocytic %, and phagocytic index) was noticed by FM replacement with KBH. The cumulative mortality as a result of challenging with Aeromonas sobria at the end of the feeding trial was decreased by increasing the replacement level (80, 40, 37, 30, and 25% for KBH0, KBH25, KBH50, KBH75, and KBH100, respectively). From the economic point of view, the feed costs and feed cost/ kg gain declined in the KBH75 and KBH100 diets. From the aforementioned outcomes, KBH could replace the FM up to 100% with improving the growth and their related genes expression, digestive enzymes activity, and immune/antioxidant parameters and their encoding gene expression, and the optimal replacement level was 76%. The replacement of FM with KBH was economically efficient.

Effects of dietary trimetlylamine oxide on the growth performance, feed utilization and appetite regulation of Chinese mitten crab (Eriocheir sinensis)

A 60-day feeding trial was conducted to evaluate the effects of different TMAO (trimetlylamine oxide) supplement levels (0%, 0.12%, 0.24%, and 0.48%, named G1, G2, G3, and G4, respectively) on growth performance, feed utilization, intestinal enzyme activities and appetite regulation of Eriocheir sinensis. The results showed that diet supplemented with 0.24% trimetlylamine oxide (TMAO) significantly improved the weight gain rate (WGR), specific growth rate (SGR), feed intake (FI) and feed utilization (p < 0.05), while having no effect on the survival rate (SR) and molting frequency (MF) of crabs (p > 0.05). Moreover, moderate dietary TMAO levels significantly improved the intestinal enzyme activities (α-amylase, trypsin, lipase and γ-glutamyl transferase) of crabs. The RT-qPCR results showed that the expressions of the orexigenic neural signal-related factors neuropeptide Y (npy) and ghrelin were significantly up-regulated. The expressions of AKT/TOR/4E-BP signaling pathway related genes (protein kinase B (akt), target of rapamycin (tor) and 4E-binding protein (4e-bp)), anorexia-regulating peripheral hormones (leptin and cholecystokinin (cck)) and leptin receptor (lepr) were significantly down-regulated in the hepatopancreas, thoracic ganglia and cranial ganglia tissues. The anorexigenic neural signal-related factors cocaine and amphetamine regulated transcript (cart) and pro-opiomelanocortin (pomc) were significantly down-regulated in the hepatopancreas, thoracic ganglia and cranial ganglia tissues. Based on the quadratic regression analysis of WGR against dietary TMAO level, the optimum TMAO requirement of E. sinensis was suggested to be 0.27%. In conclusion, present results suggested that dietary supplementation with 0.27% TMAO can improve the growth performance, feed intake, intestinal enzyme activities and appetite regulation of E. sinensis.

Exploring the effects of adiponectin and leptin in correlating obesity with cognitive decline: a systematic review.

Obesity and cognitive decline including dementia and Alzheimer's Disease (AD) affect millions worldwide. Several studies have shown that obese individuals suffer from cognitive decline. Here, we suggest that adiponectin and leptin, protein hormones secreted by white adipose tissue explain the relationship between obesity and cognitive decline. We systematically searched PubMed and World Health Organization (WHO) websites with the keywords obesity and dementia and compiled literature that explains how adiponectin and leptin impact obesity and cognitive decline. Full-text, free-access articles on PubMed published after 2009 have been included. Whereas articles published before 2009, books, and reports were excluded. We concentrated on mechanisms via which adiponectin and leptin affect energy expenditure, fatty acid catabolism, satiety, hunger, Body Mass Index (BMI), neurogenesis, and brain structures that lead to the development of cognitive dysfunction. Moreover, we hypothesized that adiponectin and leptin hormones explain how obesity and dementia are connected. After compiling the research studies, we summarized that adiponectin and leptin negatively correlate to BMI. Adiponectin arbitrates energy expenditure and fatty acid catabolism to prevent obesity. In the presence of adiponectin, hippocampal cells proliferate, whereas neurogenesis is reduced in its absence. However, leptin prevents obesity by promoting satiety, reducing hunger, and increasing insulin sensitivity. It also has neuroprotective effects thus reducing the risk of developing cognitive decline. So, physical exercise, diet alteration, weight reduction, adiponectin, and leptin supplementation should be carried out to protect against obesity-induced cognitive decline. Therefore, further research studies should be done in this area.

Is hyperleptinemia associated with gallstone disease? A systematic review and meta-analysis.

Obesity is one of the risk factors for gallstone disease (GD). Leptin hormone is known to regulate central obesity. Thus, hyperleptinemia may also be involved in gallstone disease pathogenesis. In the present study, a meta-analysis was performed to compare the leptin levels in GD and controls. The authors reviewed studies till April 12, 2021, which reported the serum leptin levels in gallstone patients and healthy controls. The online search involved ScienceDirect and PubMed databases. The data obtained from the research articles was scrutinized for selection criteria. Only those articles which fulfilled the inclusion criteria were subjected to meta-analysis. Of 2047 articles, a total of eight studies met the inclusion and exclusion criteria and were considered for the meta-analysis. After meta-analysis, it was observed that the patients with GD had high leptin levels as compared to healthy controls. A significant level of heterogeneity was observed in the included studies (I2 = 89%, p < 0.01). There was no publication bias. High leptin levels might be involved in GD pathogenesis.

Sleep Patterns, Eating Behavior and the Risk of Noncommunicable Diseases.

Sleep is extremely important for the homeostasis of the organism. In recent years, various studies have been carried out to address factors related to sleep patterns and their influence on food choices, as well as on the onset of chronic noncommunicable diseases. The aim of this article is to provide a scientific literature review on the possible role of sleep patterns on eating behavior and the risk of noncommunicable diseases. A search was performed on Medline (PubMed interface) using several keywords (e.g., "Factors Influencing Sleep" OR "Sleep and Chronic Diseases"). Articles published between 2000 and the present date that relate sleep to cyclic metabolic processes and changes in eating behavior were selected. Changes in sleep patterns are increasingly detected today, and these modifications are mainly caused by work and lifestyle conditions as well as a growing dependence on electronic devices. Sleep deprivation and the resultant short sleep duration lead to an increased appetite via an increase in the hunger hormone (ghrelin) and a decrease in the satiety hormone (leptin). Nowadays, sleep is undervalued, and thus often impaired, with consequences for the performance of various body systems. Sleep deprivation alters physiological homeostasis and influences eating behavior as well as the onset of chronic diseases.

Intrarenal Anti-Leptin Treatment Attenuates Ischemia and Reperfusion Injury

Introduction: Renal ischemia and reperfusion (IR) injury introduces cellular stress and is the main cause of acute kidney damage. Renal cells exposed to noxious stress induce the expression of the pleiotropic hormone leptin. As we have previously revealed a deleterious stress-related role for leptin expression, these results suggested that leptin is also involved in pathological renal remodeling. The systemic functions of leptin preclude the study of its local effects using conventional approaches. We have therefore designed a method to locally perturb leptin activity in specific tissues without affecting its systemic levels. This study explores whether local anti-leptin strategy is renoprotective in a post-IR porcine kidney model. Methods: We induced renal IR injury in pigs by exposing kidneys to ischemia and revascularization. Upon reperfusion, kidneys instantly received an intra-arterial bolus of either a leptin antagonist (LepA) or saline solution. Peripheral blood was sampled to assess systemic leptin, IL-6, creatinine, and BUN levels, and postoperative tissue samples were analyzed by hematoxylin and eosin histochemistry and immunohistochemistry. Results: Histology of IR/saline kidneys exhibited extensive necrosis of proximal tubular epithelial cells, as well as elevated levels of apoptosis markers and inflammation. In contrast, IR/LepA kidneys showed no signs of necrosis or inflammation with normal IL-6 and tall-like receptor 4 levels. LepA treatment led to upregulation in mRNA levels of leptin, leptin receptor, ERK1/2, STAT3, and transport molecule Na/H exchanger-3. Conclusions: Local, intrarenal postischemic LepA treatment at reperfusion prevented apoptosis and inflammation and was renoprotective. Selective intrarenal administration of LepA at reperfusion may provide a viable option for clinical implementation.

Metabolic hormone action in the VTA: Reward-directed behavior and mechanistic insights

Dysfunctional signaling in midbrain reward circuits perpetuates diseases characterized by compulsive overconsumption of rewarding substances such as substance abuse, binge eating disorder, and obesity. Ventral tegmental area (VTA) dopaminergic activity serves as an index for how rewarding stimuli are perceived and triggers behaviors necessary to obtain future rewards. The evolutionary linking of reward with seeking and consuming palatable foods ensured an organism's survival, and hormone systems that regulate appetite concomitantly developed to regulate motivated behaviors. Today, these same mechanisms serve to regulate reward-directed behavior around food, drugs, alcohol, and social interactions. Understanding how hormonal regulation of VTA dopaminergic output alters motivated behaviors is essential to leveraging therapeutics that target these hormone systems to treat addiction and disordered eating. This review will outline our current understanding of the mechanisms underlying VTA action of the metabolic hormones ghrelin, glucagon-like peptide-1, amylin, leptin, and insulin to regulate behavior around food and drugs of abuse, highlighting commonalities and differences in how these five hormones ultimately modulate VTA dopamine signaling.