Plasma Leptin Levels Research Articles

Establishing a Female Animal Model of Prediabetes Using a High-Carbohydrate, High-Fat Diet

Prediabetes is a condition that often precedes the onset of type 2 diabetes and is characterized by moderate levels of insulin resistance. This condition is well established in male animal models for diabetes; however, few female models exist. There is accumulating evidence that sex variations affect the pathogenesis, treatment, and consequences of numerous diseases, such as type 2 diabetes. Therefore, we sought to develop a diet-induced prediabetic female animal model to better understand prediabetes development and its effects in females. Female Sprague Dawley rats were randomly allocated to one of two groups: the standard diet (SD) group fed a standard diet with normal drinking water, and the high-carbohydrate, high-fat (HCHF) group fed a high-carbohydrate and high-fat diet with drinking water supplemented with fructose. During induction, we measured food intake, body weight, body mass index (BMI), and oral glucose tolerance response (OGT). After the induction period, biochemical analyses were conducted to assess the levels of plasma leptin, ghrelin, insulin, and glycated hemoglobin (HbA1c). Glycogen concentrations were quantified in the liver and skeletal muscles. The HCHF diet-fed group presented higher body weight gain, food intake, and BMI levels, which were accompanied by elevated plasma insulin, ghrelin, and liver and skeletal muscle glycogen levels compared to the SD-fed group. In the HCHF diet-fed group, the HOMA-IR was above 1.9, suggesting the presence of moderate levels of insulin resistance. The OGT response was significantly higher in the HCHF-fed group versus the SD-fed group, suggesting impaired glucose tolerance, thus displaying the signs and symptoms of prediabetes. The HCHF diet with fructose led to the induction of prediabetes in female Sprague Dawley rats. This model could be used to investigate and outline the pathophysiological complications associated with prediabetes in females as a result of the prolonged ingestion of a high carbohydrate, high-fat diet with fructose. The development of this model could also serve as an effort to further bridge the gap regarding the inclusion of females in biomedical research, thus providing advancements in deriving better, specified treatment strategies for women.

Regional and ethnic factors of obesity and diabetes mellitus in women of re-productive age in the Pribaikal region

Introduction. Overweight is currently one of the leading global medical problems. Overweight and obesity contribute significantly to the development of diseases such as diabetes, cardiovascular disorder and can also cause premature death. Obesity has a negative impact on reproductive function; almost a quarter of women of childbearing age are overweight and about a third of them are obese.Aim. To study the characteristics of carbohydrate metabolism, hormonal indicators, and clinical-metabolic profiles, as well as to assess the potential risk of developing diabetes mellitus in women of fertile age with overweight and obesity residing in the Baikal region.Materials and methods. The study involved 60 overweight and obese women of reproductive age in the Pribaikalye region, including 33 women of Russian nationality (group 1) and 27 women of Buryat nationality (group 2). Anthropo-metric, sociodemographic and behavioural criteria were analysed, as well as questionnaires using the FINDRISC Scale. General clinical analyses of blood and urine were performed, lipid profile parameters, glucose, insulin, creatinine, transaminases, estradiol, thyroid hormone, leptin levels in blood plasma were studied. In addition, an oral glucose tolerance test was performed and the insulin resistance index (HOMA-IR) was calculated.Results. In the group of Buryat women with lower body weight as compared to Russians, higher levels of leptin, HOMA- IR index, and larger waist circumference are observed. In Buryat women, low physical activity makes a significant contribution to the development of overweight and obesity, while for Russian women, excessive caloric intake is more important. In accordance with the results of the FINDRISC scale survey, the greatest contribution to the potential development of diabetes mellitus in the Russian group is body mass index (weight), and in the Buryat group, in addition to these indicators, waist circumference and reduced physical activity.Conclusions. The results of the study will be of great help in the development of pro-grammes for the prevention of diabetes and obesity, taking into account regional and ethnic differences among the population.

Postnatal surge of adipose-secreted leptin is a robust predictor of fat mass trajectory in mice.

The transient postnatal increase in circulating leptin levels, known as leptin surge, may increase later susceptibility to diet-induced obesity in rodents. However, the source of leptin during the surge needs to be better characterized, and the long-term effects of leptin are contradictory. Characterization of the interaction of leptin with the genetic background, sex, and other factors is required. Here, we focused on the impact of circulating leptin levels and several related variables, measured in 2- and 4-week-old (i) obesity-prone C57BL/6 (B6) and (ii) obesity-resistant A/J mice. In total, 264 mice of both sexes were used. Posttranscriptionally controlled leptin secretion from subcutaneous white adipose tissue, the largest adipose tissue depot in mice pups, was the primary determinant of plasma leptin levels. When the animals were randomly assigned standard chow or high-fat diet (HFD) between 12 - 24 weeks of age, the obesogenic effect of HFD-feeding was observed in B6 but not A/J mice. Only leptin levels at 2 weeks, i.e., close to the maximum in the postnatal leptin surge, correlated with both body weight (BW) trajectory throughout the life and adiposity of the 24-week-old mice. Leptin surge explained 13 and 7 % of the variance in BW and adiposity of B6 mice and 9 and 35 % of the variance in these parameters in A/J mice, with a minor role of sex. Our results prove the positive correlation between the leptin surge and adiposity in adulthood, reflecting the fundamental biological role of leptin. This role could be compromised in obese subjects.

Plasma leptin levels are lower in females, but not males, with ketamine use disorder

ABSTRACT Background: Ketamine has emerged as a prominent substance of misuse. Leptin, an adipocyte-derived polypeptide hormone, has been implicated in the development of addiction. Sex-specific changes in leptin levels have been demonstrated following acute ketamine administration; the persistence of long-term ketamine use on leptin levels is uncertain. Objectives: To assess the sex-difference of leptin levels, and their persistence, in individuals with ketamine use disorder (KUD) compared to healthy controls. Methods: Plasma leptin levels were measured in 62 healthy controls (37 males, 25 females) and 68 participants with KUD (50 males, 18 females) on the first day (baseline) and after 1 and 2 weeks of abstinence. As leptin levels are affected by body mass index (BMI), BMI-adjusted leptin (leptin/BMI ratio) was also examined. Mixed model for repeated measures was used to examine changes after ketamine abstinence. Results: Compared to same-sex controls, female, but not male, participants with KUD demonstrated lower leptin levels and leptin/BMI ratio at baseline, week 1, and week 2 (leptin levels: p = .001, 0.006 and 0.032, respectively; leptin/BMI ratio: p = .004, 0.022, and 0.09, respectively). Repeated measures showed that leptin levels and the leptin/BMI ratio increased after 2 weeks of abstinence in male participants with KUD (p = .002 and 0.011, respectively), but females did not show such an increase (p > .05). Conclusions: Sex-specific differences were observed in leptin levels and the leptin/BMI ratio in individuals with KUD compared to controls. Lower leptin levels in females with KUD persisted after 2 weeks of abstinence.

Association between overweight and central interleukin-6 in a nonclinical adult population.

Overweight is associated with low-grade systemic inflammation. However, its effect on neuroinflammation remains unclear. We examined the possible association between overweight and neuroinflammation using cerebrospinal fluid (CSF) in a nonclinical adult population in Japan. CSF and plasma levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), plasma levels of C-reactive protein (CRP), and leptin were measured in nonclinical adult participants (35 males and 34 females) who had no current or past history of neuropsychiatric diseases. We performed partial correlation analyses with sex and age as covariates between the body mass index (BMI) and the inflammatory markers and compared them between overweight and nonoverweight participants. The BMI significantly correlated with CSF levels of IL-6 (rs = 0.32, p = 0.009), plasma levels of CRP (rs = 0.30, p = 0.016), IL-1β (rs = 0.29, p = 0.019), IL-6 (rs = 0.25, p = 0.042), TNF-α (rs = 0.43, p < 0.001), and leptin (rs = 0.72, p < 0.001). Overweight participants (BMI ≧ 25) had significantly higher CSF levels of IL-6 (p < 0.001), plasma levels of IL-1β (p = 0.023), TNF-α (p < 0.001), and leptin (p < 0.001) than the nonoverweight participants. Overweight is associated with central IL-6, a marker for neuroinflammation, as well as systemic inflammation markers, even in a nonclinical population.

Maternal Diet during Pregnancy Alters the Metabolites in Relation to Metabolic and Neurodegenerative Diseases in Young Adult Offspring

Maternal nutrition during the critical period of pregnancy increases the susceptibility of offspring to the development of diseases later in life. This study aimed to analyze metabolite profiles to investigate the effect of maternal diet during pregnancy on changes in offspring plasma metabolites and to identify correlations with metabolic parameters. Pregnant Sprague-Dawley rats were exposed to under- and overnutrition compared to controls, and their offspring were fed a standard diet after birth. Plasma metabolism was profiled in offspring at 16 weeks of age using liquid chromatography–mass spectrometry (LC-MS/MS) and gas chromatography–tandem mass spectrometry (GC-MS/MS). We analyzed 80 metabolites to identify distinct metabolites and metabolic and neurodegenerative disease-associated metabolites that were sex-differentially altered in each group compared to controls (p &lt; 0.05, VIP score &gt; 1.0). Specifically, changes in 3-indolepropionic acid, anthranilic acid, linoleic acid, and arachidonic acid, which are involved in tryptophan and linoleic acid metabolism, were observed in male offspring and correlated with plasma leptin levels in male offspring. Our results suggest that fatty acids involved in tryptophan and linoleic acid metabolism, which are altered by the maternal diet during pregnancy, may lead to an increased risk of metabolic and neurodegenerative diseases in the early life of male offspring.

Association of polymorphic variants of the leptin gene with anthropometric and biochemical parameters in adolescents with different weight status

The leptin gene (LEP) is considered as a potential candidate gene affecting metabolic disorders associated with predisposition to overweight and obesity.The aim of the study. To search for single nucleotide polymorphisms (SNP) of the leptin gene and to assess their relationship with anthropometric and biochemical parameters in Russian and Buryat adolescents with different weight status.Materials and methods. The study included adolescents of two ethnic groups – Caucasoid (Russians) and Mongoloids (Buryats) – aged 11–17 years (mean age 14.8 ± 0.45 years) with different weight status. We assessed anthropometric parameters, determined biochemical parameters and leptin level in the blood plasma, and sequenced the leptin gene fragment localized in the 128253475–128255334 region (1859 bp) of this gene using the Sanger method.Results. The sequencing of the leptin gene fragment identified 10 single nucleotide substitutions (rs28954118, rs3828942, rs759854910, rs199893150, rs7788818, rs144755411, rs917105894, chr7:128255051, chr7:128255092, chr7:128254681), two of them (rs28954118, rs144755411) had a correlation with biochemical and anthropometric parameters. In the group of Russian adolescents with overweight and/or obesity, the carriers of the AT variant of rs28954118 had statistically significantly higher levels of triglycerides (TG), very low density lipoprotein (VLDL) cholesterol, skin fold thickness on the abdomen and fat mass percentage compared with carriers of the AA genotype. In the control group of Buryat adolescents, the parameters of waist width, skin fold thickness on the hip and waist width/height ratio are statistically significantly lower in carriers of the CT variant of rs144755411 compared with carriers of the CC genotype.Conclusion. AT genotype of rs28954118 was identified only in Russian adolescents with overweight and/or obesity, and was accompanied with statistically significantly high values of TG, VLDL cholesterol, skin fold thickness on the abdomen and fat mass percentage. The SNPs we identified do not affect the concentration of leptin.

Abstract 68: Soluble FMS-Like Tyrosine Kinase 1 induces Vascular Endothelial Dysfunction in Pregnant Female Mice

Preeclampsia (PE) is a hypertensive disorder of pregnancy clinically characterized by hypertension and increased risk of fetal growth restriction. Elevated levels of anti-angiogenic soluble fms-like tyrosine kinase 1 (sFlt-1) is a well-known hallmark of PE. In addition, emerging clinical evidence indicates that vascular endothelial dysfunction is a mediator of PE. Although these two facets of PE are associated, whether sFlt-1 is a crucial mediator in endothelial dysfunction in PE is unknown. We previously showed that the placenta-derived hormone leptin, whose levels characteristically increase in PE patients, induces the features of PE in pregnant mice, notably endothelial dysfunction. Novel preliminary data also shows that sFlt-1 induces an increase in placental leptin production, however, what remains to be explored is whether this pathway mediates endothelial dysfunction in PE pregnant mice. Therefore, we hypothesize that in pregnant mice, sFlt-1 induces vascular endothelial dysfunction via increasing leptin production. We bred BALB/c female mice for timed pregnancy (12-14 wk old). On gestational day (GD)11, pregnant females were implanted with subcutaneous (sc.) minipumps containing either sFlt-1 (1.2 µg/day, n=5) or saline (n=6). Uterine artery resistance index (UARI) was measured at GD17 via Doppler ultrasound. At GD18, vascular reactivity was measured in 2nd-order mesenteric arteries by wire myography. Our data showed that sFlt-1 increased UARI compared to sham mice ([PSV-EDV]/PSV; Mean±SEM;0.61±0.01 vs. 0.45±0.01, t test, p=0.0007). In addition, sFlt-1 reduced endothelial-dependent relaxation to acetylcholine (concentration-response, 1nM-10µM, 2-way ANOVA w/RM, p&lt;0.0001), indicating endothelial dysfunction. sFlt-1 also reduced smooth muscle relaxation responses to sodium nitroprusside (p&lt;0.05). To test whether sFlt-1 induces leptin production, we bred BALB/c mice as described above. At GD12, mice were treated with either sFlt-1 (sc.10 µg) or saline (n=6/group). After 24 h, mice were euthanized, and plasma and subcutaneous adipose tissue were collected. Our data showed an increase in plasma leptin in sFlt-1 group (ng/mL;5.0 ±0.2 vs. 2.9±0.1, t test, p&lt;0.0001) and an upregulation in placental leptin gene expression (normalized to 18S; fold change to control; 7.8±1.8 vs. 1.1±0.3, t test, p&lt;0.05). In conclusion, our data indicates that sFlt-1 induces vascular endothelial dysfunction and increases leptin plasma levels and gene expression in preeclampsia.

Metabolic Changes Following Smoking Cessation in Patients with Type 2 Diabetes Mellitus.

Smoking cessation is crucial for reducing complications of type 2 diabetes mellitus (T2DM), but associated weight gain can worsen glycemic control, discouraging quitting attempts. Varenicline, a partial agonist of α4β2 nicotinic receptors, aids smoking cessation. This study examines the effects of varenicline on body weight and metabolic parameters in patients with T2DM and prediabetes. Fifty-three patients were enrolled, of which 32 successfully quit smoking after a three-month course of varenicline and were examined after an additional month with no medication. Measurements taken at baseline, 2.5 months, and 4 months included body weight, blood pressure, resting metabolic rate (RMR), glycated hemoglobin (HbA1c), fasting glucose, blood lipids, C-reactive protein (CRP), appetite-related hormones, and physical activity. Post-treatment, there were no significant changes in body weight, blood pressure, RMR, or glycemic control. Total (CHOL) and low-density lipoprotein (LDL-C) cholesterol decreased significantly at 4 months of the study (from 168 to 156 mg/dL, p = 0.013, and from 96 to 83 mg/dL, p = 0.013, respectively). Leptin levels increased (from 11 to 13.8 ng/dL, p = 0.004), as did glucagon-like peptide-1 (GLP-1) levels (from 39.6 to 45.8 pM, p = 0.016) at 4 months of follow-up. The percentage of participants who reported moderate-intensity activity increased from 28% to 56%, while those reporting high-intensity activity increased from 19% to 22%, respectively (p = 0.039). Our study showed that smoking cessation with varenicline in smokers with T2DM and prediabetes led to significant improvements in lipid profile, significant increase in plasma leptin and GLP-1 levels, and increased physical activity, without significant weight gain. Thus, smoking cessation without weight gain or deteriorated glycemic control is feasible for these smokers, with added benefits to lipid profiles, GLP-1 regulation, and physical activity.

Effects of Repeated Administration of Rauwolfia Serpentina on Stress-Induced Anorexia and Leptin Levels: Relationship With Adaptation to Stress

Background: Stress is a major contributor to various health issues, including depression, anorexia nervosa, diabetes, and obesity. Rauwolfia serpentina, a traditional medicinal plant, has shown potential in alleviating stress-induced effects due to its influence on serotonin neurotransmission and its anxiolytic properties. Objective: This study aimed to investigate the effects of repeated administration of Rauwolfia serpentina on stress-induced anorexia and leptin levels, and its relationship with adaptation to stress in rats. Methods: Male albino Wistar rats were divided into four groups: DMSO unstressed, DMSO stressed, Rauwolfia serpentina unstressed, and Rauwolfia serpentina stressed. The stressed groups were subjected to two hours of immobilization daily for five days, followed by oral administration of Rauwolfia serpentina at 10 mg/kg. Behavioral assessments included the open field and light-dark transition tests. Body weight, food intake, and plasma levels of glucose, leptin, and corticosterone were measured. Data were analyzed using ANOVA with post-hoc Newman-Keuls test, and significance was set at p&lt;0.05. Results: Rauwolfia serpentina significantly improved body weight maintenance (98.9 ± 1.3% vs. 99.5 ± 1.7%) and increased food intake (16.3 ± 0.6 g vs. 16.5 ± 0.5 g) in stressed rats. It also reduced anxiety-like behaviors and lowered corticosterone levels (15.9 ± 1.6 ng/mL vs. 18.4 ± 1.7 ng/mL) in stressed groups (p&lt;0.05). Conclusion: Rauwolfia serpentina effectively alleviates stress-induced anorexigenic and anxiogenic effects, suggesting its potential as a therapeutic agent for managing stress-related disorders.

Thermoneutrality Inhibits Thermogenic Markers and Exacerbates Nonalcoholic Fatty Liver Disease in Mice.

Nonalcoholic fatty liver disease (NAFLD) affects over a third of the US population and 25% globally, with current treatments proving ineffective. This study investigates whether manipulating brown adipose tissue (BAT) and beige fat activity by housing C57BL/6J mice at thermoneutral (27 °C) or standard temperatures (22 °C) impacts NAFLD development. Male mice were fed either a chow diet (CHD) or a "fast food" diet (FFD) for 10 weeks. Mice at 27 °C had reduced food intake but increased body weight and plasma leptin levels. FFD-fed mice at 27 °C had greater liver weight (2.6 vs. 1.8 g), triglyceride content (7.6 vs. 3.9 mg/g), and hepatic steatosis compared to those at 22 °C. Gene expression of fatty acid synthase, sterol regulatory element-binding protein 1, and fatty acid translocase CD36 was elevated in FFD-fed mice at 27 °C, but not in CHD-fed mice. Thermoneutral housing also reduced expression of thermogenic markers in BAT and inguinal white adipose tissue (WAT) and caused BAT whitening. In conclusion, thermoneutrality inhibits thermogenic markers and exacerbates NAFLD. Activating BAT or promoting WAT browning via cold exposure or other stimuli may offer a strategy for managing NAFLD.

Impact of Resistance and Endurance Training on Ghrelin and Plasma Leptin Levels in Overweight and Obese Subjects.

Exercise training is a valuable tool for improving body weight and composition in overweight or obese adults, which leads to a negative energy balance. It is relevant to consider whether exercise can help people lose weight or prevent weight gain because any energy expended in exercise increases the severity of hunger and promotes food consumption. Over the past decade, the identification of the circulating peptide ghrelin, which alerts the brain to the body's nutritional state, has significantly expanded our understanding of this homeostatic mechanism that controls appetite and body weight. To shed more light on this issue, we decided to investigate the effects of resistance and endurance training on plasma ghrelin and leptin levels. In addition, we sought to understand the mechanisms by which acute and chronic exercise can regulate hunger. This review analyzes studies published in the last fifteen years that focused on changes suffered by ghrelin, leptin, or both after physical exercise in overweight or obese individuals. Most studies have shown a decrease in leptin levels and an increase in ghrelin levels in these cases. Exercise regimens that support weight maintenance need further investigation.

Anti-obesity effect of standardized ethanol extract from the leaves of Adenocaulon himalaicum Edgew. via regulation of adipogenesis and lipid accumulation in 3T3-L1 cells and high-fat diet-induced obese mice

Obesity causes various complications like type 2 diabetes and fatty liver, and as the proportion of obese patients increases worldwide, the discovery of new treatments has become necessary. Here, we evaluated the in vitro and in vivo anti-obesity effects of 30% ethanol extract of Adenocaulon himalaicum Edgew. (EEAH). Treatment with EEAH suppressed adipogenesis and lipogenesis via the AMP-activated protein kinase (AMPK) pathway. EEAH altered the expression of adipogenic and lipogenic proteins and impeded mitotic clonal expansion during adipocyte differentiation. Oral administration of EEAH significantly mitigated body weight gain and fat accumulation in high-fat diet-induced obese mice. EEAH regulated adipogenesis and lipid accumulation in white adipose and liver tissues. EEAH modulated plasma levels of insulin and leptin. In brown adipose tissue, EEAH induced expression of thermogenic factors. EEAH shows potential for treating obesity by reducing body weight, inhibiting lipid accumulation, and suppressing adipogenesis through the AMPK pathway.

Adipokine modulation in obesity: Evaluating the integrative impact of chlorella vulgaris supplementation and interval resistance training in obese males

AimsTo evaluate the effects of 12-week chlorella vulgaris (CV) combined with interval resistance training (IRT) on plasma levels of leptin, adiponectin and neuregulin-4 (Nrg-4) in obese men. MethodsObese men (n = 44, BMI of 32.1 ± 1.5 kg/m2) were randomly allocated to the following groups of 11 participants per group: Control Placebo group (CP), CV supplement group (CV), Interval Resistance Training group plus Placebo (IRT + P), and Interval Resistance Training plus CV supplement group (IRT + CV). IRT was performed three times a week for 12 weeks using three sets of 10 repetitions at 60 % 1RM, and integrating an active rest interval with 15 repetitions at 20 % 1RM. Participants consumed either CV (1800 mg daily) or a placebo. Pre- and post-intervention blood samples were obtained to assess adipokines which were measured by ELISA. ResultsWhile CV or IRT separately did not alter plasma levels of leptin (p > 0.05), their combination reduced leptin levels (p = 0.007). IRT and IRT plus CV increased the plasma levels of adiponectin and Nrg-4 (p < 0.01). An intergroup comparison indicated significant elevations of adiponectin and Nrg-4 in the CV compared to the CP group (p < 0.05). ConclusionThe combination of IRT and CV modulates plasma levels of leptin, adiponectin and NRG4 more effectively than either IRT or CV separately in obese men.

Short-term feeding of high-fat diet induces neuroinflammation and oxidative stress in arcuate nucleus in rats

Objectives: This study aimed to compare the effects of high-fat diet-induced neuroinflammation and oxidative stress in the arcuate nucleus (ARC) of obese-prone and obese-resistant rats. Materials and Methods: Rats were divided into obese-prone and obese-resistant groups based on their initial body weight. They were then fed either a 5% or 60% fat-containing diet. In the ARC, the expression of inflammatory markers [Interleukin (IL-6); Nuclear Factor Kappa-B Inhibitor Alpha (NFKBIA); Cluster of Differentiation (CD)-66; and mucin-like hormone receptor-like 1 (EMR-1)], as well as levels of reactive oxygen species (ROS) and antioxidant enzymes (glutathione and glutathione peroxidase and superoxide dismutase), was assessed along with body weight, blood glucose, Homeostatic Model Assessment for Insulin Resistance, plasma insulin and plasma leptin levels after ten days of intervention. Results: The results showed a significantly higher expression of inflammatory markers in the ARC of high-fat diet-induced obese rats after ten days. Body weight, plasma insulin, plasma leptin and hydrogen peroxide production were also significantly higher in obese-prone rats fed a high-fat diet. Conclusion: In conclusion, this study demonstrates that short-term consumption of a high-fat diet can lead to hypothalamic inflammation and ROS production in the ARC of rats. Obese-prone rats exhibited hyperinsulinaemia and hyperleptinaemia after short-term high-fat diet consumption.

Concurrent strength and aerobic exercise reduce plasma leptin and cortisol levels

To analyze the correlation between leptin and cortisol after a concurrent training (CT) session. Thirty male volunteers (age: 27.7 ± 5.1 years, BMI: 27.08 ± 1.42 kg/m2) were randomly assigned to an experimental group (EG: n=15) and a control group (CG: n=15). Baseline leptin and cortisol levels were determined by collecting blood samples. EG was subjected to CT (indoor cycling followed by strength training), whereas CG performed no exercise. After CT, blood samples were collected in EG and CG to determine the hormone variables. EG showed a significant decrease (p&lt;0.05) intra and intergroup in leptin and cortisol levels. Only the EG showed a significant correlation (r=0.756; p&lt;0.05) between leptin and cortisol levels. CT session is linked to in decreased leptin and cortisol levels, exhibiting a positive correlation between them.

Metabolic Responses to High-Fat Feeding and Chronic Psychological Stress Combination.

High-fat diet (HFD) consumption and being exposed to daily psychological stress, common environmental factors in modern lifestyle, play an important role on metabolic disorders such as glucose homeostasis impairment. The aim of this study was to investigate the effects of high-fat diet (HFD) and psychological stress combination on metabolic response to chronic psychological stress in male rats. Male Wistar rats were divided into HFD, and normal diet (ND) groups and then into stress and nonstress subgroups. The diets were applied for 5 weeks, and psychological stress was induced for 7 consecutive days. Then, blood samples were taken to measure glucose, insulin, free fatty acids (FFA), and leptin and corticosterone concentrations. Subsequently, glucose-stimulated insulin release from pancreatic isolated islets was assessed. HFD did not significantly change fasting plasma glucose, insulin and corticosterone levels, whereas increased plasma leptin (7.05 ± 0.33) and FFA (p < 0.01) levels and impaired glucose tolerance. Additionally, HFD and stress combination induced more profound glucose intolerance associated with increased plasma corticosterone (p < 0.01) and leptin (8.63 ± 0.38) levels. However, insulin secretion from isolated islets did not change in the presence of high-fat diet and/or stress. HFD should be considered as an intensified factor of metabolic impairments caused by chronic psychological stress.

Peripheral inflammatory hyperalgesia is exacerbated in rats with metabolic disorders induced by a fructose diet.

This study explored the effects of fructose-induced obesity and metabolic disorders on peripheral inflammatory hyperalgesia, employing quantitative sensory testing with the von Frey test and measuring paw edema to assess inflammatory responses. Wistar rats were administered water or 10% fructose solution ad libitum over a period of 5 weeks. After intraplantar administration of inflammatory agents such as carrageenan (1 mg/paw), lipopolysaccharide (LPS; 100 µg/paw), or prostaglandin E2 (PGE2, 100 ng/paw), we conducted mechanical hyperalgesia tests and paw edema evaluations. The fructose diet resulted in dyslipidemia, elevated insulin and leptin plasma levels, insulin resistance, and increased epididymal and retroperitoneal adiposity compared to control animals. In response to inflammatory agents, the fructose group displayed significantly enhanced peripheral hyperalgesia and more pronounced paw edema. Our results demonstrate that fructose not only contributes to the development of obesity and metabolic disorder but also exacerbates peripheral inflammatory pain responses by enhancing prostaglandin sensitivity.

Maternal choline supplementation mitigates premature foetal weight gain induced by an obesogenic diet, potentially linked to increased amniotic fluid leptin levels in rats.

Placental leptin may impact foetal development. Maternal overnutrition has been linked to increased plasma leptin levels and adverse effects on offspring, whereas choline, an essential nutrient for foetal development, has shown promise in mitigating some negative impacts of maternal obesity. Here, we investigate whether a maternal obesogenic diet alters foetal growth and leptin levels in the foetal stomach, amniotic fluid (AF), and placenta in late gestation and explore the potential modulating effects of maternal choline supplementation. Female rats were fed a control (CD) or a western diet (WD) four weeks before mating and during gestation, half of them supplemented with choline (pregnancy days 11-17). Leptin levels (in foetal stomach, AF, and placenta) and leptin gene expression (in placenta) were assessed on gestation days 20 and 21. At day 20, maternal WD feeding resulted in greater leptin levels in foetal stomach, placenta, and AF. The increased AF leptin levels were associated with a premature increase in foetal weight in both sexes. Maternal choline supplementation partially prevented these alterations, but effects differed in CD dams, causing increased AF leptin levels and greater weight in male foetuses at day 20. Maternal choline supplementation effectively mitigates premature foetal overgrowth induced by an obesogenic diet, potentially linked to increased AF leptin levels. Further research is needed to explore the sex-specific effects.

Body fat and circulating leptin levels in the captive short-beaked echidna (Tachyglossus aculeatus)

It is possible that the reproductive strategy of the short-beaked echidna is related to seasonal changes in fat deposition and energy availability, regulated by seasonal changes in endocrine function. We predicted that circulating leptin levels would be directly proportional to adiposity during most of the year, but that a change in this relationship would occur during the pre-breeding season to allow increased fat deposition. To test this hypothesis, we made use of a captive colony of echidnas to describe and quantify changes in fat distribution and the adipostatic hormone leptin. First we assessed seasonal changes in circulating leptin levels, body mass and adiposity for three male and three female adult echidnas maintained on a standard diet. Second, we explored the relationship between circulating leptin levels and increased caloric intake for an additional five adult female echidnas that were provided with supplemented nutrition. Third we visualised fat distribution in male and female adult echidnas using magnetic resonance imaging (MRI) before and after the breeding season, to determine where fat is deposited in this species. For echidnas maintained on the standard diet, there were no seasonal changes in body mass, body fat or plasma leptin levels. However, female echidnas provided with supplemented nutrition had significantly elevated plasma leptin levels during the breeding season, compared to the pre-and post- breeding periods. MRI showed substantial subcutaneous fat depots extending dorso-laterally from the base of the skull to the base of the tail, in both sexes. Pre-breeding season, both sexes had considerable fat deposition in the pelvic/rump region, whilst the female echidna accumulated most fat in the abdominal region. This study shows that male and female echidnas accumulate body fat in the pelvic/rump and the abdominal regions, respectively and that circulating leptin may promote fattening in female echidnas during the breeding season by means of leptin resistance. However, further research is required to evaluate the precise relationship between seasonal changes in leptin and adiposity.