Serum Leptin Concentrations Research Articles

Low Molecular Weight Barley β-Glucan Affects Glucose and Lipid Metabolism by Prebiotic Effects.

We investigated the effect of low molecular weight barley β-glucan (LMW-BG) on cecal fermentation, glucose, and lipid metabolism through comparisons to high molecular weight β-glucan (HMW-BG). C57BL/6J male mice were fed a moderate-fat diet for 61 days. LMW-BG or HMW-BG was added to the diet corresponding to 4% β-glucan. We measured the apparent absorption of fat, serum biomarkers, the expression levels of genes involved in glucose and lipid metabolism in the liver and ileum, and bacterial counts of the major microbiota groups using real time PCR. The concentration of short-chain fatty acids (SCFAs) in the cecum was analyzed by GC/MS. Significant reductions in serum leptin, total- and LDL-cholesterol concentrations, and mRNA expression levels of sterol regulatory element-binding protein-1c (SREBP-1c) were observed in both BG groups. HMW-BG specific effects were observed in inhibiting fat absorption and reducing abdominal deposit fat, whereas LMW-BG specific effects were observed in increasing bacterial counts of Bifidobacterium and Bacteroides and cecal total SCFAs, acetate, and propionate. mRNA expression of neurogenin 3 was increased in the LMW-BG group. We report that LMW-BG affects glucose and lipid metabolism via a prebiotic effect, whereas the high viscosity of HMW-BG in the digestive tract is responsible for its specific effects.

Sleep Disturbance Induces Increased Cholesterol Level by NR1D1 Mediated CYP7A1 Inhibition.

Disturbed sleep is closely associated with an increased risk of metabolic diseases. However, the underlying mechanisms of circadian clock genes linking sleep and lipid profile abnormalities have not been fully elucidated. This study aimed to explore the important role of the circadian clock in regulating impaired cholesterol metabolism at an early stage of sleep deprivation (SD). Sleep disturbance was conducted using an SD instrument. Our results showed that SD increased the serum cholesterol levels. Concentrations of serum leptin and resistin were much lower after SD, but other metabolic hormone concentrations (adiponectin, glucagon, insulin, thyroxine, norepinephrine, and epinephrine) were unchanged before and after SD. Warning signs of cardiovascular diseases [decreased high density lipoprotein (HDL)-cholesterol and increased corticosterone and 8-hydroxyguanosine levels] and hepatic cholestasis (elevated total bile acids and bilirubin levels) were observed after SD. Cholesterol accumulation was also observed in the liver after SD. The expression levels of HMGCR, the critical enzyme for cholesterol synthesis, remained unchanged in the liver. However, the expression levels of liver CYP7A1, the enzyme responsible for the conversion of cholesterol into bile acids, significantly reduced after SD. Furthermore, expression of NR1D1, a circadian oscillator and transcriptional regulator of CYP7A1, strikingly decreased after SD. Moreover, NR1D1 deficiency decreased liver CYP7A1 levels, and SD could exacerbate the reduction of CYP7A1 expression in NR1D1−/− mouse livers. Additionally, NR1D1 deficiency could further increase serum cholesterol levels under SD. These results suggest that sleep disturbance can induce increased serum cholesterol levels and liver cholesterol accumulation by NR1D1 mediated CYP7A1 inhibition.

Dietary Enrichment with Omega -3 Fatty Acid Potentiates Leptin Permeability through the Blood-Brain Barrier in Wistar Rats

Obesity is an excessive accumulation of fat which causes several health implications. It is a risk factor for most disabilities and non-communicable diseases such as cardiovascular diseases, diabetes, cancer, neurodegenerative diseases, etc. The present study aimed to show the effect of short and long-term supplementation of an enriched diet with different concentrations of omega-3 fatty acid on cerebrospinal fluid (CSF), and serum leptin ratio, adiposity and lipid profile in albino Wistar rats. Serum-leptin ratios and indicators such as lipid profile, feed consumption, and adiposity index were obtained to ascertain the effect of the enriched diet on health and wellness. Forty Wistar rats divided into four groups of ten were used, comprising of five males and females; Groups A, B, C and D. The group A, the control, was fed with rat chow and water alone. Groups B, C and D were fed with rat chow supplemented with 10%, 20% and 40% omega-3 fatty acid respectively. The permeability of the blood-brain barrier (BBB) with leptin significantly increased across the experimental groups in a concentration-dependent manner.
 Practical Applications: Omega-3-fatty acids, also called polyunsaturated fatty acids are well known for their cardioprotective properties. ALA, α-linoleic acid, eicosapentanoic acid (EPA), and docosahexanoic acid (DHA) have been collectively referred to as omega-3 fatty acids. ALA, an essential fatty acid, can be converted into EPA and DHA. These polyunsaturated fatty acids (PUFA) are obtained from fish-oil and other kinds of seafood. Dietary consumption is essential for a better blood lipid profile and reduced risk for cardiovascular disease. In the present study, supplementation with omega-3 fatty acids improved blood-lipid profile, increased HDL which are essential in preventing obesity. Equally reported here is that concentrations of serum-leptin and CSF were used to derive the leptin ratio. There was also a significant decrease in the adiposity index across the groups. The feed consumption and CSF leptin were given as r=-0.46 for the short term diet, while r=0.34 for the long term diet group. Data of the study indicate that omega-3 fatty acid enrichment had a diminishing effect on both adiposity and appetite, but enhanced the permeability of leptin through the blood-brain barrier in the Wistar rats. The relevance of this study is that omega-3-fatty acid food supplementation could aid in weight management and assist in the prevention and control of obesity.

Adiponectin/leptin ratio increases after a 12-week very low-carbohydrate, high-fat diet, and exercise training in healthy individuals: A non-randomized, parallel design study

This study aimed to investigate the effect of a 12-week very low-carbohydrate, high-fat (VLCHF) diet and exercise on biomarkers of inflammation in healthy individuals. Since the anti-inflammatory effects of a ketogenic diet have been established, we hypothesized that the VLCHF diet, along with exercise, would have an additional favorable effect on biomarkers of inflammation. Twenty-four healthy individuals were allocated to the VLCHF diet (VLCHF: N = 12, age 25.3 ± 2.0 years, body mass 66.7 ± 9.8 kg, fat mass 21.5% ± 4.9%), or habitual diet (HD: N = 12, age 23.9 ± 3.8 years, body mass 72.7 ± 15.0 kg, fat mass 23.4 ± 8.4 %) group. Biomarkers of inflammation (adiponectin, leptin, and high-sensitive interleukin-6 [hs-IL-6]) and substrate metabolism (glycated hemoglobin, fasting glucose, triacylglycerides, and cholesterol) were analyzed from blood at baseline and after 12 weeks. The adiponectin-leptin ratio significantly increased in the VLCHF group after the intervention period (ES [95% CL]: −0.90 [−0.96, −0.77], P ≤ .001, BF10 = 22.15). The adiponectin-leptin ratio changes were associated with both a significant increase in adiponectin (−0.79 [−0.91, −0.54], P ≤ .001, BF10 = 9.43) and a significant decrease in leptin (0.58 [0.19, 0.81], P = .014, BF10 = 2.70). There was moderate evidence of changes in total cholesterol (−1.15 [−2.01, −0.27], P = .010, BF10 = 5.20), and LDL cholesterol (−1.12 [−2.01, −0.21], P = .016, BF10 = 4.56) in the VLCHF group. Body weight (kg) and fat mass (%) decreased in the VLCHF group by 5.4% and 14.9%, respectively. We found that in healthy young individuals, consuming a VLCHF diet while performing regular exercise over a 12-week period produced favorable changes in body weight and fat mass along with beneficial changes in serum adiponectin and leptin concentrations. These data support the use of a VLCHF diet strategy for the primary prevention of chronic diseases associated with systemic low-grade inflammation.

60 Effects of exogenous glucocorticoid administration on leptin concentrations in perinatal dairy bull calves

Abstract Previous studies suggest a relationship between leptin and cortisol immediately postpartum is linked to improved feedlot efficiency on cattle exposed to perinatal stressors. The objective of the current study was to determine the effects of exogenous cortisol administration on circulating leptin concentrations in perinatal dairy bull calves. Within four hours of parturition, Holstein bull calves were randomly assigned to treatments and intravenously infused with low cortisol (LC; n =9, 3.5 ug/kg of cortisol), high cortisol (HC; n = 9, 7.0 ug/kg of cortisol), or a sham infusion control (CON; n = 9, similar volume of saline). Calves were housed similarly and fed milk replacer (28% CP, 20% fat) three times daily. Blood collections were performed via jugular venipuncture using Z/9mL serum collection tubes (Sarstedt, Newton, NC) from d 0 to 5 of age. Serum samples were incubated for 1 h at room temperature then overnight at 4°C, centrifuged at 1800 x g at 4°C for 20 minutes, serum decanted, and stored long term at -20°C until analysis. At 5 d of age, calves were euthanized utilizing an overdose of sodium pentobarbital (Schering-Plough Animal Health, Union, NJ) and cerebral-spinal fluid (CSF) from the third ventricle of the brain was collected and stored at -80°C until analysis. All samples were analyzed for leptin concentrations via a previously-validated radioimmunoassay. Serum leptin concentrations were analyzed via repeated measures of ANOVA and CSF leptin concentrations via the GLM procedure of SAS (SAS Institute Inc., Cary, NC, USA). Serum leptin concentrations of HC and LC were decreased (P = 0.013) compared to CON, and d 0 was decreased (P < 0.001) compared to all other days of age. Cerebral-spinal fluid leptin concentrations of HC and LC were decreased (P = 0.005) compared to CON. In summary, exogenous cortisol administered to perinatal dairy bull calves reduced leptin concentrations in serum and CSF.

59 Effects of exogenous glucocorticoid administration on leptin concentrations in perinatal dairy bull calves

Abstract Previous studies suggest a relationship between leptin and cortisol immediately postpartum is linked to improved feedlot efficiency on cattle exposed to perinatal stressors. The objective of the current study was to determine the effects of exogenous cortisol administration on circulating leptin concentrations in perinatal dairy bull calves. Within four hours of parturition, Holstein bull calves were randomly assigned to treatments and intravenously infused with low cortisol (LC; n = 9, 3.5 ug/kg of cortisol), high cortisol (HC; n = 9, 7.0 ug/kg of cortisol), or a sham infusion control (CON; n = 9, similar volume of saline). Calves were housed similarly and fed milk replacer (28% CP, 20% fat) three times daily. Blood collections were performed via jugular venipuncture using Z/9mL serum collection tubes (Sarstedt, Newton, NC) from d 0 to 5 of age. Serum samples were incubated for 1 h at room temperature then overnight at 4°C, centrifuged at 1800 x g at 4°C for 20 minutes, serum decanted, and stored long term at -20°C until analysis. At 5 d of age, calves were euthanized utilizing an overdose of sodium pentobarbital (Schering-Plough Animal Health, Union, NJ) and cerebral-spinal fluid (CSF) from the third ventricle of the brain was collected and stored at -80°C until analysis. All samples were analyzed for leptin concentrations via a previously-validated radioimmunoassay. Serum leptin concentrations were analyzed via repeated measures of ANOVA and CSF leptin concentrations via the GLM procedure of SAS (SAS Institute Inc., Cary, NC, USA). Serum leptin concentrations of HC and LC were decreased (P = 0.013) compared to CON, and d 0 was decreased (P < 0.001) compared to all other days of age. Cerebral-spinal fluid leptin concentrations of HC and LC were decreased (P = 0.005) compared to CON. In summary, exogenous cortisol administered to perinatal dairy bull calves reduced leptin concentrations in serum and CSF.

Degree of Agreement Between Infant Serum and Salivary Concentration of Leptin and Adiponectin and Its Association With Infants' Feeding.

Leptin and adiponectin, two adipokines involved in glucose and lipid metabolism, have been linked to regulation of growth in early infancy, energy balance, and metabolic disorders in childhood. The aim of this study was to determine if concentrations of leptin and adiponectin could be measured reliably in infants' saliva, to evaluate the degree of agreement with infant serum levels, and to explore their association with infant feeding status. A total of 34 infants were recruited after birth and followed for 20 weeks. After log-transformation of the values, a Bland-Altman graphical approach was used to summarize the direction of the difference between the serum and saliva values. Repeated measures mixed modeling was used to evaluate differences over time in these outcomes by feeding status. Mean concentration of salivary leptin and adiponectin in infants was 3.7 (SD = .8) ng/mL and 2.9 (SD = 0.7) ng/mL, respectively. The degree of agreement between serum and saliva for log-transformed leptin and adiponectin values were relatively robust, albeit with a non-zero bias between the two methods, given that serum values were greater than corresponding saliva values for both adipokines in all infants. Each of the four repeated measures mixed models (one for each adipokine measure) had a significant main effect; however, the interaction between time and feeding status was not significant in any of the models. This study demonstrated that leptin and adiponectin can be measured in infant saliva, but in some cases leptin concentrations may be more difficult to detect.

Antiobesity effects of kimchi added with Jeju citrus concentrate on high-fat diet-induced obese mice

Citrus fruits contain an abundance of nutrients, including vitamins C and B6 and hesperidin, which attribute to its beneficial health effects. Previously, kimchi with Jeju citrus concentrate (CK) elicited anti-obesity effects in 3T3-L1 adipocytes. Here, we aimed to investigate whether CK exhibits anti-obesity effects by reducing serum and hepatic lipid concentrations and anti-obesity-associated gene expression in high-fat diet (HFD)-induced obese C57BL/6N mice. Low-dose CK (LDCK, 50 mg/kg) and high-dose CK (HDCK, 200 mg/kg) were orally administered 3 times per week over 8 weeks with HFD diet. Body weight gain, food efficiency ratio, and tissue weight were measured. Serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, fasting glucose, fasting insulin, homeostatic model assessment-insulin resistance, leptin, and adiponectin concentrations were also assessed. The effect of CK on the lipid profile and lipid accumulation was analyzed. Body and white adipose tissue masses were significantly lower in the LDCK and HDCK groups than in the HFD group. Orally administered CK significantly decreased serum lipid, fasting glucose, fasting insulin, homeostatic model assessment-insulin resistance, glutamic oxaloacetic transaminase, and glutamic pyruvic transaminase levels. Hepatic lipid content also decreased in the LDCK and HDCK groups. Serum leptin concentrations decreased, whereas serum adiponectin concentrations increased, confirming the anti-obesity effects of LDCK and HDCK. The decrease of hepatic vacuoles and stained lipid droplets indicated inhibition of lipid accumulation. These results support the hypothesis that CK exhibits anti-obesity effects in vivo by reducing lipid accumulation and by regulating anti-obesity-related genes.

Sfrp5/Wnt5a and leptin/adiponectin levels in the serum and the periarterial adipose tissue of patients with peripheral arterial occlusive disease

BackgroundLeptin, adiponectin, secreted frizzled-related protein 5 (Sfrp5) and wingless-type family member 5a (Wnt5a) are novel adipokines that are involved in insulin sensitivity and atherosclerosis. The aim of the present study was to investigate the serum and periarterial adipose tissue leptin/adiponectin and Sfrp5/Wnt5a levels in patients with peripheral arterial occlusive disease (PAOD). MethodsA total of 75 patients with PAOD and 39 control subjects were recruited. The serum concentrations of leptin, adiponectin, Sfrp5 and Wnt5a were measured by ELISAs, and the leptin, adiponectin, Sfrp5 and Wnt5a levels in the periarterial adipose tissue were observed by western blotting. ResultsThe serum Sfrp5 levels were significantly lower in the patients with PAOD than in the control subjects (p < 0.001) and Wnt5a levels were higher in the patients with PAOD (p < 0.001). The serum leptin levels were significantly higher in the patients with PAOD than in the control subjects (p < 0.001), and adiponectin levels were significantly lower in the patients with PAOD (p < 0.001). The serum Sfrp5 levels were associated with ABI (rs = 0.274; p = 0.018), Wnt5a (rs = −0.409; p < 0.001), adiponectin (rs = 0.244; p = 0.035) and Leptin/Adiponetin ratio (rs = −0.244; p = 0.037). The adiponectin and Sfrp5 protein levels were decreased in the periarterial adipose tissue of patients with PAOD compared with control subjects. The leptin and Wnt5a protein levels were increased in the periarterial adipose tissue of patients with PAOD compared with control subjects. ConclusionWe demonstrated that the adiponectin and Sfrp5 levels in the serum and periarterial adipose tissue were significantly lower in the patients with PAOD than in the control subjects. The leptin and Wnt5a levels in the serum and periarterial adipose tissue were significantly higher in the patients with PAOD than in the control subjects.

Association of leptin serum concentration with heart adipose tissue and parameters of systolic and diastolic function in heart failure patients

Abstract Aims Leptin has recently been related to myocardial remodeling in animal experimentation studies on heart failure (HF). Furthermore, leptin has been reported to be related to diastolic dysfunction, however only in healthy population. With the emergence of new medical therapies targeting cardiac remodeling, there needs to be a better understanding of the metabolic pathways involving leptin. Our study aims to investigate leptin's correlation to parameters of systolic and diastolic heart function, as well as epicardial and pericardial adipose tissue (EAT and PAT) in heart failure (HF) patients. Methods The study included 51 patients with chronic heart failure with reduced ejection fraction (HFrEF) of ischemic (n=22) and non-ischemic (n=29) origin (NYHA II-III, mean EF 29.56%, SD 8.1; mean BMI 28.08, SD 5.8). Serum concentrations of leptin, NT-proBNP, HbA1c, LDL, and total cholesterol were also measured. Global longitudinal strain (GLS) and other LV function parameters were assessed in transthoracic echocardiography, as well as EAT and PAT in parasternal long and short-axis views. Results We found a significant correlation between leptin serum concentration and epicardial, as well as pericardial adipose tissue (EAT r=0.336, p=0.030; PAT r=0.565, p&amp;lt;0.001). There was a significant negative correlation between leptin and GLS (r=−0.332; p=0.045), as well a positive correlation between Leptin and E/E' ration (r=0.373; p=0.039). There was no significant difference between ischemic and non-ischemic HF patients. Conclusion We provide evidence of serum leptin correlation to remodeling parameters, as well as epicardial and pericardial fat tissue in HF patients. Whether leptin has positive effects on reversing or preventing remodeling in heart failure, needs further investigation. Correlation of leptin vs. GLS Funding Acknowledgement Type of funding source: None

Differing planes of pre- and postweaning phase nutrition in Holstein heifers: II. Effects on circulating leptin, luteinizing hormone, and age at puberty

The objectives were to investigate the effects of differing planes of pre- and postweaning nutrition on prepubertal serum leptin concentrations, LH profiles, and age at puberty in Holstein heifers. Thirty-six Holstein calves were randomly assigned to either a low (5 L) or high (10 L of whole milk/d) preweaning plane of nutrition from 1 to 7 wk of age, a transition diet (a dry total mixed ration with 85% of concentrate) from wk 8 to 10, and to either a low (70%) or high (85% of concentrate dry total mixed ration) postweaning plane from 11 to 25 wk of age. Serum leptin concentrations were measured every 2 wk from 1 to 25 wk of age, and LH profiles were determined both at wk 15 and 25 based on sequential blood samples taken every 12 min over 10 h. Starting at 26 wk of age, ovaries were examined weekly by transrectal ultrasonography until first ovulation (puberty) was confirmed. Heifers that received the high preweaning plane diet had greater mean (± standard error; SE) leptin concentrations during the preweaning phase than those fed the low plane (2.9 ± 0.1 vs. 2.6 ± 0.1 ng/mL). During the postweaning phase, mean circulating leptin was greater in heifers fed the high compared with the low postweaning diet [3.2 ng/mL (95% confidence interval; CI = 2.7 to 3.4) vs. 2.5 ng/mL (95% CI = 2.3 to 2.8)]. Mean (± SE) amplitude (2.1 ± 0.1 vs. 1.7 ± 0.1 ng/mL), peak (2.2 ± 0.1 vs. 1.8 ± 0.1 ng/mL), and duration (35.6 ± 2.1 vs. 28.7 ± 2.0 min) of LH pulses assessed at wk 15 were greater in heifers offered the high than those offered the low preweaning plane, but no nutritional effects were observed on LH pulses at wk 25. Mean (± SE) age at puberty was 250 ± 9 d and was not influenced by planes of nutrition. However, the likelihood of attaining puberty by 30 wk of age was greater (hazard ratio = 3.8; 95% CI = 1.0 to 14.4) in heifers fed the high postweaning plane compared with the low plane. Heifers achieving puberty by 30 wk also had greater leptin concentrations from wk 1 to 25, whereas for every 1 ng/mL increase in circulating leptin at wk 15 and 25, days to puberty were estimated to decrease by 22 d (95% CI = 1 to 44) and 13 d (95% CI = 1 to 24), respectively. Increasing the preweaning plane from 5 to 10 L/d of whole milk increased serum leptin concentrations at wk 1, 3, and 5 and LH pulse amplitude, peak, and duration at wk 15. Increasing the postweaning plane from 70 to 85% of concentrate resulted in greater circulating leptin concentrations, which may be linked to an earlier onset of puberty.

Changes in Appetite Regulation-Related Signaling Pathways in the Brain of Mice Supplemented with Non-nutritive Sweeteners

Non-nutritive sweeteners (NNSs) are commonly used to prevent weight gain and development of metabolic diseases associated with consumption of high-energy diets. Recent studies have demonstrated that these compounds may have unwanted detrimental effects under specific circumstances in vivo. In particular, an association between NNS consumption and changes in signaling pathways involved in the hunger-satiety system in the brain has been reported. Nonetheless, the extent of alterations in brain signaling pathways associated with consumption of these compounds has not been determined. The objective of this study was to determine the effect of frequent consumption of NNSs on the expression of proteins involved in signaling pathways related to appetite control in the brain in vivo. Eight-week-old BALB/c mice were supplemented with sucrose, sucralose, or steviol glycosides in their daily drinking water for 6weeks. Subsequently, total brain protein extracts were used to analyze the expression of total and phosphorylated JAK2, STAT5, ERK 1/2, JNK, as well as SHP-2 and POMC, by western blot. Serum concentrations of leptin and α-MSH were quantified by ELISA. Results show that consumption of NNSs promotes significant changes in these signaling pathways, reducing the expression of pSTAT5/STAT5, pERK 1/2, SHP-2, and pJNK/JNK in male mice supplemented with steviol glycosides. Furthermore, consumption of steviol glycosides induced a decrease of α-MSH in male mice. In contrast, steviol glycosides induced overexpression of pSTAT5, pERK, and SHP-2 in females. These data suggest that chronic consumption of NNSs promotes sex-specific changes in signaling pathways related to the central hunger-satiety system in vivo.

The influence of fasting and energy-restricted diets on leptin and adiponectin levels in humans: A systematic review and meta-analysis

Fasting and energy-restricted diets have been evaluated in several studies as a means of improving cardiometabolic biomarkers related to body fat loss. However, further investigation is required to understand potential alterations of leptin and adiponectin concentrations. Thus, we performed a systematic review and meta-analysis to derive a more precise estimate of the influence of fasting and energy-restricted diets on leptin and adiponectin levels in humans, as well as to detect potential sources of heterogeneity in the available literature. A comprehensive systematic search was performed in Web of Science, PubMed/MEDLINE, Cochrane, SCOPUS and Embase from inception until June 2019. All clinical trials investigating the effects of fasting and energy-restricted diets on leptin and adiponectin in adults were included. Twelve studies containing 17 arms and a total of 495 individuals (intervention=249, control=246) reported changes in serum leptin concentrations, and 10 studies containing 12 arms with a total of 438 individuals (intervention=222, control=216) reported changes in serum adiponectin concentrations. The combined effect sizes suggested a significant effect of fasting and energy-restricted diets on leptin concentrations (WMD:-3.690ng/ml, 95% CI:-5.190,-2.190, p≤0.001; I2=84.9%). However, no significant effect of fasting and energy-restricted diets on adiponectin concentrations was found (WMD:-159.520ng/ml, 95% CI:-689.491, 370.451, p=0.555; I2=74.2%). Stratified analyses showed that energy-restricted regimens significantly increased adiponectin (WMD: 554.129ng/ml, 95% CI: 150.295, 957.964; I2=0.0%). In addition, subsequent subgroup analyses revealed that energy restriction, to ≤50% normal required daily energy intake, resulted in significantly reduced concentrations of leptin (WMD:-4.199ng/ml, 95% CI:-7.279,-1.118; I2=83.9%) and significantly increased concentrations of adiponectin (WMD: 524.04ng/ml, 95% CI: 115.618, 932.469: I2=0.0%). Fasting and energy-restricted diets elicit significant reductions in serum leptin concentrations. Increases in adiponectin may also be observed when energy intake is ≤50% of normal requirements, although limited data preclude definitive conclusions on this point.

Hypothermic Effect of Acute Citral Treatment during LPS-induced Systemic Inflammation in Obese Mice: Reduction of Serum TNF-α and Leptin Levels.

Citral is a mixture of monoterpenes present in the essential oil of several plants, such as Cymbopogon citratus and Zingiber officinale, possessing anti-inflammatory, anti-ulcerogenic, and antipyretic actions. We investigated the action of citral on body temperature (Tb) and inflammatory signaling in eutrophic and obese mice during Systemic Inflammation (SI) induced by Lipopolysaccharide (LPS). Thus, we assessed the effect of citral (25, 100, and 300 mg/kg) and ibuprofen in LPS-induced SI in Swiss male mice fed a standard diet (SD) or high-fat diet (HFD) for 12 weeks. Following SI induction, we measured Tb and collected the serum, hypothalamus, and gastric mucosa for biochemical measurements. Acute treatment with citral decreased the Tb of both SD and HFD-fed animals. Citral (300 mg/kg) treatment caused a significantly lower Tb variation in HFD-fed animals than in those fed the SD. Citral reduced peripheral levels of tumor necrosis factor (TNF)-α in SD and HFD mice and decreased serum leptin concentration in HFD mice 90 min after the LPS challenge. Furthermore, citral also reduced interleukin (IL)-6 levels in the hypothalamus of obese mice. In summary, citral effectively reduced Tb during SI by reducing inflammatory mediators with a distinct action profile in HFD mice when compared with SD.

Association of Leptin Promoter 2548G/A variant with Serum Leptin, Lipid Profile and Type 2 Diabetes Mellitus

Background: A common 2548G/A promoter variant of the human leptin gene has been implicated in circulating leptin levels variations and pathogenesis of type 2 diabetes mellitus but available data are still conflicting. Objective: To explore potential associations between LEP 2548G/A of leptin with T2DM and the effect of this variation on serum leptin levels. Patients and Methods: Sixty two patients with T2DM and fifty non-diabetic controls were included in the study. Blood samples were collected from subjects for biochemical analysis and Genotyping was performed by polymerase chain reaction reaction–restriction fragment length polymorphism (PCR-RFLP). Results: The genotype frequencies for LEP 2548G/G, LEP 2548G/A LEP 2548A/A were 46%, 32% and 22% in control group, and 19.4%, 33.9% and 46.7% in diabetic group, respectively. The A allele and GA/AA genotype of LEP 2548G/A was found to be more frequent than the G allele and GG genotype in T2DM patients compares to the controls. Subjects with the GA + AA genotype of LEP 2548G/A were at increased risk for T2DM (P=0.0001, OR = 1.78; 95% CI: 1.19–2.38). The serum leptin concentration of GA + AA genotype carriers was significantly higher from that of the GG genotype in the diabetic group. Conclusion: A allele carrier who have higher serum concentrations of leptin may have an association with the risk of T2DM development in the Erbi population.

Maternal Occupational Tobacco Exposure and Newborn Umbilical Cord Serum Leptin Concentration

To assess the effect of maternal occupational tobacco handling (bidi rolling) on cord serum leptin levels. We enrolled 64 neonates born to women who were bidi-rollers, and 64 small for gestational age (SGA) neonates and 57 term appropriate for gestational age (AGA) neonates born to mothers with no tobacco exposure. Cord blood leptin levels between the groups were compared. Adjusted mean difference in leptin was calculated using regression model. Cord leptin showed moderate correlation with birthweight (r=0.16; P=0.027) across the groups. Mean (SD) cord serum leptin levels (ng/mL) of study group was 19.79 (13.32), in comparison to 21.4 (13.4) of SGA (P=0.497), and 27.70 (13.96) of term AGA (P=0.002). Maternal occupational tobacco exposure contributed to significant decrease in cord leptin (adjusted mean difference (95%CI): -4.5 ng/mL (-8.82, -0.19); P=0.041). Maternal occupational tobacco exposure causes signifi-cant reduction in fetal leptin levels.

Maternal serum leptin, adiponectin, resistin and monocyte chemoattractant protein-1 levels in different types of diabetes mellitus

ObjectiveEvaluation of serum concentration of leptin, adiponectin, resistin, and MCP-1 in pregnant patients with different types of diabetes mellitus (DM) considering preconception planning and method of DM correction in 11–14th and 30–34th weeks of pregnancy. Study designLongitudinal, prospective study included 130 pregnant women divided into the following comparison groups: type 1 DM (T1DM, n = 40), type 2 DM (T2DM, n = 35), GDM (n = 40), and the control group (n = 15). The ELISA method defined the levels of leptin, resistin, adiponectin, and MCP-1 concentration in serum, which was assessed in 11–14th and 30–34th weeks of pregnancy. Statistical analysis was accomplished using SPSS 23.0 and "Prism 8-GraphPad" software. ResultsThe leptin level in the 1st trimester was the highest in T2DM insulin group compared to the control due to gestational age, hence in the 3rd trimester in all groups its serum concentrations appeared higher than in healthy patients (p = 0.0001). In the 1st trimester leptin levels directly correlated with women's BMI, newborns’ weight and macrosomia rate, in the 3rd trimester – with OGTT levels, HbA1c, gestational hypertension, and preeclampsia rates. Resistin levels in the 1st and 3rd trimesters were increased in almost all DM groups compared to the control group (p = 0.0001). The study established direct positive correlation between resistin and HbA1c, birth weight, and preeclampsia. In the 1st trimester, adiponectin demonstrated the lowest levels in T2DM insulin compared to T1DM and the control group (p = 0.0001) while in the 3rd trimester, adiponectin levels declined alongside gestational age in DM patients and all the groups compared to the control group (p < 0.05). Adiponectin negatively correlated with BMI, OGTT levels, and preeclampsia rate. MCP-1 levels in T2DM appeared higher than in T1DM patients and the control group in the 1st trimester, whereas in the 3rd trimester MCP-1 declined, correlating with BMI, preeclampsia and OGTT levels. ConclusionHigh rate of adverse perinatal outcomes in diabetic pregnancy might be developed due to more severe metabolic failures and further disturbances of adipokines expression.

Association between obesity-associated markers and semen quality parameters and serum reproductive hormones in Chinese infertile men

BackgroundThe current evidence on the association between obesity-associated markers and semen quality, serum reproductive hormones and lipids remains inconsistent. In this study, we tested the hypothesis that, in infertile Chinese men, body mass index (BMI) negatively correlates with sperm concentration, serum total testosterone (TT), and high-density lipoprotein cholesterol (HDL-C). The relationship between other obesity-associated markers and semen quality parameters, serum reproductive hormones, lipids and leptin were also investigated.Methods181 Chinese infertile men were recruited from September 2018 to September 2019. Their obesity-associated markers, semen parameters, and serum reproductive hormones, lipids and leptin were detected. Statistical analysis was performed to assess the relationship between obesity-associated markers and semen quality, serum reproductive hormones, lipids and leptin.Result(s)Statistically negative correlation was found between other obesity-associated markers (e.g. waist-to-hip ratio and waist-to-height ratio) and semen parameters (e.g. sperm concentration, ratio of progressive motility and ratio of non-progressive motility), while no significant correlation was found between BMI and semen quality, serum reproductive hormones, lipids and leptin. Ratio of morphologically normal sperm was negatively correlated with serum lipids including total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), leptin and seminal superoxide dismutase. Ratio of progressive sperm, sperm concentration and ratio of morphologically normal sperm exhibited significantly lower values in overweight group than normal group. Estradiol (E2) and E2/TT were significantly higher in obese group than normal group, while TT level was significantly lower in obese group than normal group. Univariate and multivariate analysis indicated that TC was significantly associated with BMI. Serum leptin concentration was positively correlated with seminal leptin concentration in overweight and obese groups.Conclusion(s)No significant correlation was found between BMI and sperm concentration, serum TT and HDL-C, while other obesity-associated markers were found to negatively correlate with sperm concentration, ratio of progressive motility and ratio of non-progressive motility. Statistically significant correlations between serum reproductive hormones, lipids and leptin also existed in Chinese infertile men.

Re-evaluation of serum leptin and adiponectin concentrations normalized by body fat mass in patients with rheumatoid arthritis

Leptin and adiponectin are produced mainly in adipocytes and classified as adipocytokines because of their possible involvement in inflammation and immunity. The aim of this study was to elucidate the relationships of these adipocytokines with the disease activities of RA. We examined leptin and adiponectin concentrations and inflammatory markers such as metalloproteinase-3 (MMP-3) in 136 patients with rheumatoid arthritis (RA) (26 males and 110 females, 69.6 ± 9.3 years) and 78 controls (36 males and 42 females, 66.7 ± 15.0 years). Serum leptin and adiponectin concentrations correlated positively (r = 0.565, P < 0.001) and negatively (r = –0.331, P < 0.001) to the amount of body fat, respectively. Serum leptin and adiponectin concentrations normalized by body fat mass were significantly higher in RA than those in controls [leptin, 1.24 (median) ng/mL/kg fat in RA vs. 0.76 ng/mL/kg fat in controls; adiponectin, 0.74 μg/mL/kg fat in RA vs. 0.44 μg/mL/kg fat in controls]. Normalized adiponectin concentrations correlated positively not only to the degree of bone destruction in Steinbrocker classification but also to serum MMP-3 concentrations. Normalized leptin concentrations did not correlate to the degree of bone destruction. We conclude that adiponectin but not leptin may be involved in joint damage in RA.

Carnosic acid prevented olanzapine-induced metabolic disorders through AMPK activation.

Olanzapine, an atypical antipsychotic medication, has been associated with weight gain and metabolic toxicity, especially in long term usage. Carnosic acid (CA), a major constituent of rosemary extract, has been shown to improve metabolic abnormalities. In this experiment, the effect of CA on olanzapine-induced obesity and metabolic toxicity has been evaluated. Female Wistar rats were divided into six groups. (1) control; (2) olanzapine (5mg/kg/day, IP); (3, 4 and 5) olanzapine (5mg/kg/day, IP) plus CA (5, 10 and 20mg/kg/day, gavage) and (6) CA (20mg/kg/day, gavage). Bodyweight and food intake were measured during the study. After 14 days, mean systolic blood pressure (MSBP), glycemia, serum lipid profile, the serum concentration of leptin, insulin, AMPK, P-AMPK, and P-ACC liver protein levels were evaluated. The mean weight in the group received olanzapine increased by 4.8g at the end of the study. The average food intake was increased by olanzapine. Olanzapine increased triglyceride, fasting blood glucose (FBG), and leptin levels. It increased MSBP and down-regulated P-AMPK/AMPK ratio and P-ACC protein levels. CA (three doses) decreased body weight gain and reduced average food intake at 10 and 20mg/kg. CA especially at the highest dose decreased the changes in lipid profile, FBG, leptin level, and MSBP. P-AMPK/AMPK and P-ACC protein levels were increased by carnosic acid. In conclusion, the activation of AMPK by CA can be proposed as a key mechanism against olanzapine-induced metabolic toxicity where the activation of AMPK increases fat consumption and regulates glucose hemostasis in the liver.