• central-s-resistin
• hypertrophy
• inflammation
• insulin-resistance
• resistin

• Junta de Comunidades de Castilla-La Mancha
• Ministerio de Ciencia e Innovación
• Institutional Aids

• appetite regulation
• glucose metabolism
• leptin adiponectin
• leptin resistance
• lifestyle modification (lsm)
• neuropeptide
• serum leptin
• type 2 diabetes mellitus

• bioactive dietary components
• carbohydrate-insulin model
• energy balance model
• energy metabolism
• gut microbiota
• inflammation
• obesity

Reindeer are native to harsh northern Eurasian environments which are characterized by long and cold winters, short summers, and limited pasture vegetation. Adipose tissues play a significant role in these animals by modulating energy metabolism, immunity, and reproduction. Here, we have investigated the transcriptome profiles of metacarpal, perirenal, and prescapular adipose tissues in Even reindeer and searched for genes that were differentially expressed in male and female individuals. A total of 15,551 genes were expressed, where the transcriptome profile of metacarpal adipose tissue was found to be distinct from that of perirenal and prescapular adipose tissues. Interestingly, 10 genes, including PRDM9, which is known to have an important role in adaptation and speciation in reindeer, were always upregulated in all three tissues of male reindeer.

Many approaches have been used in the effective management of type 2 diabetes mellitus. A recent paradigm shift has focused on the role of adipose tissues in the development and treatment of the disease. Brown adipose tissues (BAT) and white adipose tissues (WAT) are the two main types of adipose tissues with beige subsets more recently identified. They play key roles in communication and insulin sensitivity. However, WAT has been shown to contribute significantly to endocrine function. WAT produces hormones and cytokines, collectively called adipocytokines, such as leptin and adiponectin. These adipocytokines have been proven to vary in conditions, such as metabolic dysfunction, type 2 diabetes, or inflammation. The regulation of fat storage, energy metabolism, satiety, and insulin release are all features of adipose tissues. As such, they are indicators that may provide insights on the development of metabolic dysfunction or type 2 diabetes and can be considered routes for therapeutic considerations. The essential roles of adipocytokines vis-a-vis satiety, appetite, regulation of fat storage and energy, glucose tolerance, and insulin release, solidifies adipose tissue role in the development and pathogenesis of diabetes mellitus and the complications associated with the disease.

• adipose
• diabetes mellitus
• insulin resistance

• Adipokines/metabolism
• Adiponectin/metabolism
• Adipose Tissue/metabolism
• Adipose Tissue, Beige/metabolism
• Adipose Tissue, Brown/metabolism
• Adipose Tissue, White/metabolism
• Animals
• Diabetes Complications/metabolism
• Diabetes Mellitus/metabolism
• Energy Metabolism/physiology
• Humans
• Insulin/metabolism
• Insulin Resistance/physiology
• Leptin/metabolism
• Obesity/metabolism

Adipose tissue is the largest endocrine organ in humans and has an important influence on many physiological processes throughout life. An increasing number of studies have described the different phenotypic characteristics of fat cells in adults. Perhaps one of the most important properties of fat cells is their ability to adapt to different environmental and nutritional conditions. Hypothalamic neural circuits receive peripheral signals from temperature, physical activity or nutrients and stimulate the metabolism of white fat cells. During this process, changes in lipid inclusion occur, and the number of mitochondria increases, giving these cells functional properties similar to those of brown fat cells. Recently, beige fat cells have been studied for their potential role in the regulation of obesity and insulin resistance. In this context, it is important to understand the embryonic origin of beige adipocytes, the response of adipocyte to environmental changes or modifications within the body and their ability to transdifferentiate to elucidate the roles of these cells for their potential use in therapeutic strategies for obesity and metabolic diseases. In this review, we discuss the origins of the different fat cells and the possible therapeutic properties of beige fat cells.

• beige adipocyte
• brown adipocyte
• diabetes mellitus
• differentiation
• obesity
• white adipocyte

• Ob-R
• airway smooth muscles
• cobaye
• guinea pig
• leptin
• leptine
• muscle lisse des voies respiratoires

• Adipokines
• Adiponectin
• Leptin
• Peripheral artery disease
• Vascular biology

Food restriction (FR) is the most commonly used intervention to prevent the overweight. However, the lost weight is usually followed by “compensatory growth” when FR ends, resulting in overweight. The present study was aimed to examining the behavior patterns and hormones mechanisms underpinning the over-weight. Energy budget and body fat content, and several endocrine markers related to leptin signals were examined in the striped hamsters under 20% FR refed by either low-fat diet (LF group) or high-fat diet (HF group). Body mass and fat content significantly regained when FR ended, and the hamsters in HF group showed 49.1% more body fat than in LF group (P < 0.01). Digestive energy intake was higher by 20.1% in HF than LF group, while metabolic thermogenesis and behavior patterns did not differed between the two groups. Gene expression of leptin receptor and anorexigenic peptides of pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript in hypothalamus were significantly up-regulated in LF group, but down-regulated in HF group. It suggests that effective leptin signals to the brain were involved in attenuation of hyperphagia in hamsters refed with LF. However, “leptin resistance” probably occurred in hamsters refed with HF, which impaired the control of hyperphagia, resulting in development of over-weight.

• ATGL
• HSL
• lipolysis
• obesity
• steatosis
• type 2 diabetes

• Glucose homeostasis
• PGC-1α
• PPARγ
• adipokines
• adiposity

• Acute lung injury
• Adiponectin
• Gene delivery
• Inflammation
• Polymeric carrier

• Digestive tract
• Fish
• Leptin
• Obesity

• Adipokines
• Angiogenesis
• Hypoxia
• Inflammation
• Lipid intermediates
• Nutrient storage

• Adipokines/metabolism
• Adipokines/physiology
• Adipose Tissue/immunology
• Adipose Tissue/metabolism
• Adipose Tissue/physiology
• Appetite/physiology
• Biological Transport
• Blood Coagulation/physiology
• Blood Vessels/physiology
• Fatty Acids/metabolism
• Fatty Acids, Nonesterified/metabolism
• Feedback, Physiological
• Glucose/metabolism
• Humans
• Hypoxia/metabolism
• Inflammation/immunology
• Insulin Resistance/immunology
• Insulin Resistance/physiology
• Lipid Metabolism
• Metabolic Diseases/immunology
• Metabolic Diseases/metabolism
• Neovascularization, Pathologic/immunology
• Neovascularization, Pathologic/metabolism

• Female
• Humans
• Menopause/metabolism
• Metabolic Syndrome/metabolism
• Polycystic Ovary Syndrome/metabolism
• Pregnancy/metabolism
• Puberty/metabolism
• Puberty, Precocious/metabolism

Evidence on the association of leptin and adiponectin and smoking is limited and discordant. Leptin and adiponectin represent the most abundant adipokines in human plasma that play crucial roles in the pathophysiology of metabolic syndrome, atherosclerosis and insulin resistance. Leptin up-regulates the expression of several pro-inflammatory cytokines and is increased upon weight gain. Adiponectin has been shown to possess insulin sensitizing, anti -inflammatory and anti-atherogenic properties and is increased upon weight reduction. Our aim was to assess the effects of smoking cessation on serum leptin and adiponectin levels.

We assessed the changes in serum leptin and adiponectin levels, serum CRP levels and BMI in apparently healthy smokers after 3 and 6 months of abstinence from smoking. Successful cessation was confirmed by an exhaled carbon monoxide measurement. 26 healthy non-smokers were recruited as controls.

Among the sample group, 32 subjects had quitted smoking at 3 months and 29 subjects at 6 months. Samples’ leptin increased significantly from baseline to three months (mean change 3.76 ng/ml [95 % CI 0.89, 6.64], p =0.012) and then decreased significantly from three to six months of smoking cessation (mean change -4,29 ng/ml [95 % CI −7.34, −6.64], p = 0.008). Samples’ adiponectin increased significantly from baseline to three months of abstinence from smoking (mean change 2.34 [95 % CI −0.05, 4.73], p −0.05). BMI was significantly increased (mean change 2.03 kg/m² [95 % CI 1.60, 2.46], p <0.05), while CRP decreased significantly from baseline to 6 months of smoking cessation (mean change −0.68 mg/dl [95 % CI −1.06, −0.30], p = 0.001).

Smoking quitters’ leptin levels appear to increase 3 months after smoking cessation and then decrease from 3 to 6 months of abstinence from smoking. Adiponectin levels increase during the first trimester of smoking cessation. The decrease in CRP levels indicates that the low grade inflammation observed in smokers is gradually restored. The alterations of serum leptin and adiponectin after 6 months of smoking cessation suggest the same but do not reach statistically significant levels. Weight gain and changes in fat distribution may attenuate the beneficial effects of smoking cessation.

• Adiponectin
• Cessation
• Leptin
• Smoking
• Tobacco

• adipokine
• adiponectin
• leptin
• obesity
• reproduction

• Adipokines/metabolism
• Animals
• Humans
• Leptin/metabolism
• Male
• Obesity/metabolism
• Reproduction/physiology

• R01 DK091841 NIDDK NIH HHS
• R01-DK091841 NIDDK NIH HHS
• R01-HL105490 NHLBI NIH HHS

• Interleukin-6
• Labrador retriever dogs
• Monocyte chemoattractant protein-1
• Tumor necrosis factor alpha

• Adipocyte
• Bile acids
• Obesity
• Taurine

• DNA damage
• Gene polymorphisms
• Morbidly obese women
• Systemic inflammation

• Adipocytes/drug effects
• Adipocytes/metabolism
• Animals
• Fatty Acid-Binding Proteins/genetics
• Fatty Acid-Binding Proteins/metabolism
• Fatty Acids/pharmacokinetics
• Gene Expression
• Gene Silencing
• Gene Transfer Techniques
• Mice
• Molecular Targeted Therapy/methods
• Obesity/drug therapy
• Obesity/metabolism
• Oligopeptides/administration & dosage
• Oligopeptides/pharmacokinetics
• Prohibitins
• RNA, Small Interfering/metabolism
• Repressor Proteins/genetics
• Repressor Proteins/metabolism
• Transfection/methods

• Estrogen
• Food intake
• G protein-coupled receptor 30
• Hypothalamus
• STAT3

• Animals
• Anorexia/physiopathology
• Base Sequence
• DNA Primers
• Estrogens/physiology
• HeLa Cells
• Humans
• Hypothalamus/physiopathology
• Mice
• Receptors, Estrogen/physiology
• Receptors, G-Protein-Coupled/physiology
• Reverse Transcriptase Polymerase Chain Reaction
• STAT3 Transcription Factor/metabolism
• Signal Transduction/physiology

• obesity
• inflammation
• renal function
• pediatrics

• Adolescent
• Body Mass Index
• Child
• Cholesterol, HDL/blood
• Cohort Studies
• Contrast Media/chemistry
• Cross-Sectional Studies
• Cytokines/blood
• Dyslipidemias/blood
• Female
• Glomerular Filtration Rate
• Humans
• Insulin/blood
• Insulin Resistance
• Iohexol/chemistry
• Leptin/blood
• Linear Models
• Male
• Multivariate Analysis
• Renal Insufficiency, Chronic/blood
• Risk Factors
• Triglycerides/blood

• R01 DK076957 NIDDK NIH HHS
• U01 DK066116 NIDDK NIH HHS
• U01 DK066174 NIDDK NIH HHS
• U24 DK066116 NIDDK NIH HHS
• DK076957 NIDDK NIH HHS
• K24 DK090070 NIDDK NIH HHS
• U01DK-082194 NIDDK NIH HHS
• U01-DK-66143 NIDDK NIH HHS
• UL1 TR001425 NCATS NIH HHS
• U01-DK-66116 NIDDK NIH HHS
• U01-DK-66174 NIDDK NIH HHS
• K24 DK078737 NIDDK NIH HHS
• U01 DK082194 NIDDK NIH HHS
• U01 DK066143 NIDDK NIH HHS

The Chinese brown frog (Rana dybowskii) is a special amphibian with one unique physiological phenomenon, which is that its oviduct expands prior to hibernation, instead of during the breeding period. In this study, we investigate the localization and expression level of PPARγ2, leptin and leptin receptor proteins in oviduct of Rana dybowskii during breeding period and pre-hibernation. There were significant variations in oviductal weight and size, with values much lower in the breeding period than in pre-hibernation. PPARγ2 was observed in stromal and epithelial cells in both periods. Leptin was immunolocalized in epithelial cells in both periods, whereas leptin receptor was detected only in stromal cells. Consistently, the protein levels of PPARγ2, leptin and leptin receptor were higher in pre-hibernation as compared to the breeding period. These results suggested that oviduct was the target organ of leptin, which may play an important paracrine role in regulating the oviductal hypertrophy during prehibernation.

This study aimed to identify changes in the level of neuropeptides among current smokers, former smokers, and individuals who had never smoked, and how smoking habits affect obesity and metabolic syndrome (MetS). Neuropeptide levels, anthropometric parameters, and metabolic syndrome diagnostic indices were determined among male workers; 117 of these had never smoked, whereas 58 and 198 were former and current smokers, respectively. The total sample comprised 373 male workers. The results obtained from anthropometric measurements showed that current smokers attained significantly lower body weight, body mass index, waist circumference, and abdominal fat thickness values than former smokers and those who had never smoked. Current smokers’ eating habits proved worse than those of non-smokers and individuals who had never smoked. The level of brain-derived neurotrophic factor (BDNF) in the neuropeptides in the case of former smokers was 23.6 ± 9.2 pg/ml, higher than that of current smokers (20.4 ± 6.1) and individuals who had never smoked (22.4 ± 5.8) (F = 6.520, p = 0.002). The level of adiponectin among former smokers was somewhat lower than that of current smokers, whereas leptin levels were higher among former smokers than current smokers; these results were not statistically significant. A relationship was found between adiponectin and triglyceride among non-smokers (odds ratio = 0.660, β value = −0.416, p < 0.01) and smokers (odds ratio = 0.827, β value = −0.190, p < 0.05). Further, waist circumference among non-smokers (odds ratio = 1.622, β value = 0.483, p < 0.001) and smokers (odds ratio = 1.895, β value = 0.639, p < 0.001) was associated with leptin. It was concluded that cigarette smoking leads to an imbalance of energy expenditure and appetite by changing the concentration of neuropeptides such as adiponectin, BDNF, leptin, and hsCRP, and influences food intake, body weight, the body mass index, blood pressure, and abdominal fat, which are risk factors for MetS and cardiovascular disease.

• Adiponectine
• BDNF
• Leptin
• Neuropeptides
• Smoking habits

• Body mass
• Food restriction
• Hypothalamus neuropeptides
• Leptin
• Striped hamster

Among obese individuals, increased sympathetic nervous system activity results in increased renin and aldosterone production, as well as renal tubular sodium reabsorption. This study determined the associations between adipokines and selected measures of the reninangiotensinogen-aldosterone system (RAAS). The sample was 1,970 men and women from the Multi-Ethnic Study of Atherosclerosis who were free of clinical cardiovascular disease at baseline and had blood assayed for adiponectin, leptin, plasma renin activity (PRA) and aldosterone. The mean age was 64.7 years and 50% were female. The mean (SD) PRA and aldosterone were 1.45 (0.56) ng/ml and 150.1 (130.5) pg/ml, respectively. After multivariable adjustment, a 1-SD increment of leptin was associated with a 0.55 ng/ml higher PRA and 8.4 pg/ml higher aldosterone (p < 0.01 for both). Although adiponectin was not significantly associated with PRA levels, the same increment in this adipokine was associated with lower aldosterone levels (−5.5 pg/ml, p = 0.01). Notably, the associations between aldosterone and both leptin and adiponectin were not materially changed with additional adjustment for PRA. Exclusion of those taking anti-hypertensive medications modestly attenuated the associations. The associations between leptin and both PRA and aldosterone were not different by gender but were significantly stronger among non-Hispanic Whites and Chinese Americans than African and Hispanic Americans (p < 0.01). The findings suggest that both adiponectin and leptin may relevant to blood pressure regulation via the RAAS, that the associations appear to be robust to anti-hypertension medication use and that the associations are likely different by ethnicity.

• body mass
• body mass index
• fat mass
• fat mass index
• lean tissue mass
• lean tissue mass index
• 25-oh vitamin d
• leptin
• bone mineral density

• Absorptiometry, Photon
• Adult
• Aged
• Aged, 80 and over
• Body Composition
• Bone Density
• Bone and Bones/metabolism
• Female
• Humans
• Leptin/blood
• Male
• Middle Aged
• Obesity/blood
• Obesity/complications
• Obesity/metabolism
• Pulmonary Disease, Chronic Obstructive/blood
• Pulmonary Disease, Chronic Obstructive/complications
• Pulmonary Disease, Chronic Obstructive/metabolism

• AMP-Activated Protein Kinases/genetics
• AMP-Activated Protein Kinases/metabolism
• Adiposity
• Adrenocortical Hyperfunction/etiology
• Age Factors
• Animals
• Animals, Inbred Strains
• Disease Models, Animal
• Female
• Gene Expression Regulation
• Hyperinsulinism/etiology
• Inflammation Mediators/metabolism
• Intra-Abdominal Fat/immunology
• Intra-Abdominal Fat/metabolism
• Intra-Abdominal Fat/pathology
• Lipid Metabolism
• Male
• Obesity/immunology
• Obesity/metabolism
• Obesity/pathology
• Obesity/physiopathology
• Random Allocation
• Sex Characteristics
• Sheep, Domestic
• TOR Serine-Threonine Kinases/genetics
• TOR Serine-Threonine Kinases/metabolism
• bcl-2-Associated X Protein/genetics
• bcl-2-Associated X Protein/metabolism

• Amino Acid Sequence
• Animals
• Antineoplastic Agents/pharmacokinetics
• Antineoplastic Agents/pharmacology
• Cell Survival/drug effects
• Dose-Response Relationship, Drug
• Drug Design
• Drug Screening Assays, Antitumor
• Female
• HT29 Cells
• Humans
• Intracellular Signaling Peptides and Proteins/metabolism
• MCF-7 Cells
• Mice
• Mice, Inbred C57BL
• Molecular Mimicry
• Peptides/pharmacokinetics
• Peptides/pharmacology
• Receptors, Leptin/antagonists & inhibitors
• Signal Transduction
• Spheroids, Cellular/drug effects
• Tissue Distribution
• Weight Gain/drug effects

Food restriction induces a loss of body mass that is often followed by rapid regaining of the lost weight when the restriction ends, consequently increasing a risk of development of obesity. To determine the physiological and behavioral mechanisms underlining the regaining, striped hamsters were restricted to 85% of initial food intake for 4 weeks and refed ad libitum for another 4 weeks. Changes in body mass, energy budget, activity, body composition and serum leptin level were measured. Body mass, body fat mass and serum leptin level significantly decreased in food-restricted hamsters, and increased when the restriction ended, showing a short “compensatory growth” rather than over-weight or obesity compared with ad libitum controls. During restriction, the time spent on activity increased significantly, which was opposite to the changes in serum leptin level. Food intake increased shortly during refeeding, which perhaps contributed to the rapid regaining of body mass. No correlation was observed between serum leptin and energy intake, while negative correlations were found in hamsters that were refed for 7 and 28 days. Exogenous leptin significantly decreased the time spent on activity during food restriction and attenuated the increase in food intake during refeeding. This suggests that low leptin in restricted animals may function as a starvation signal to induce an increase in activity behavior, and high leptin likely serves as a satiety signal to prevent activity during refeeding. Leptin may play a crucial role in controlling food intake when the restriction ends, and consequently preventing overweight.

• Animals
• Body Composition
• Cricetinae
• Eating/physiology
• Energy Intake/physiology
• Food Deprivation/physiology
• Leptin/blood
• Male
• Motor Activity/physiology
• Weight Gain
• Weight Loss

• Animals
• Cell Line, Transformed
• Cell Movement/physiology
• Kisspeptins/genetics
• Kisspeptins/metabolism
• Mice
• Mice, Knockout
• Mutation
• Reproduction/physiology
• Signal Transduction/physiology

• BB/F01936X/1 Biotechnology and Biological Sciences Research Council

• Animals
• Dihydrotestosterone/pharmacology
• Electrophysiology
• Estrous Cycle/drug effects
• Female
• Glucose Tolerance Test
• Gonadotropin-Releasing Hormone/metabolism
• Metformin/pharmacology
• Mice
• Mice, Transgenic
• Neurons/drug effects
• Neurons/metabolism
• Pregnancy
• Prenatal Exposure Delayed Effects

• F31 NS062646 NINDS NIH HHS
• U54 HD028934 NICHD NIH HHS
• U54 HD 28934 NICHD NIH HHS
• F31 NS 062646 NINDS NIH HHS

• Adiposity/physiology
• Amino Acid Sequence
• Animals
• Evolution, Molecular
• Humans
• Leptin/chemistry
• Leptin/genetics
• Leptin/physiology
• Molecular Sequence Data
• Receptors, Leptin/physiology
• Signal Transduction/physiology

• Adipose Tissue/metabolism
• Adiposity/physiology
• Adult
• Body Mass Index
• Body Weight
• Case-Control Studies
• Female
• Glutathione/blood
• Humans
• Inflammation Mediators/blood
• Interleukins/blood
• Italy
• Lipid Metabolism Disorders/blood
• Lipid Metabolism Disorders/diagnosis
• Lipid Metabolism Disorders/metabolism
• Lipid Peroxides/blood
• Lipids/blood
• Nitric Oxide/blood
• Obesity/metabolism
• Oxidative Stress
• Reference Values
• Tumor Necrosis Factor-alpha/blood
• Waist Circumference