scholarly journals Free leptin index and thyroid function in male highly trained athletes

2009 ◽  
Vol 161 (6) ◽  
pp. 871-876 ◽  
Author(s):  
Gianluca Perseghin ◽  
Guido Lattuada ◽  
Francesca Ragogna ◽  
Giampietro Alberti ◽  
Antonio La Torre ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Thyroid Function ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Anaerobic Power ◽  
Biologically Active ◽  
Retinol Binding Protein ◽  
Endocrine Function ◽  
Whole Body ◽  
Retinol Binding Protein 4

ObjectiveExercise training may cause changes in thyroid function. This thyroid response may be due to exercise-induced modulation of energy metabolism but also of the adipocytes endocrine function. In particular, the role of leptin and of circulating soluble leptin receptor (sOB-R) was unexplored. The aim of this study was to assess the relationships between thyroid function, whole body energy metabolism, and adipokines – mainly leptin and its receptor, sOB-R.MethodsWe measured serum TSH, free tri-iodothyronine (FT3), free thyroxine, leptin, and sOB-R and assessed energy homeostasis by means of indirect calorimetry, in 27 highly trained athletes and 27 sedentary, healthy men.ResultsTSH–FT3 ratio was lower in athletes (P<0.03), either in sustained power or anaerobic power-sprint athletes (n=13) or marathon runners (n=14). Whole body respiratory quotient was lower in athletes. Fasting serum sOB-R was higher and leptin lower in athletes than controls. Also serum adiponectin, resistin, and retinol binding protein-4 concentrations were different in athletes than in controls. The ratio between leptin and sOB-R, the free leptin index (FLI), was lower in athletes than in controls (0.025±0.014 vs 0.085±0.049; P<0.001). In multivariate analysis, FLI retained independent association with TSH–FT3 ratio.ConclusionMale, elite athletes had lower TSH–FT3 ratio and FLI than controls while FLI was independently associated with TSH–FT3 ratio supporting the hypothesis that the level of biologically active leptin is involved in the adaptive response of thyroid function in professional athletes.

Abstract P247: Gut Microbiota From A Rat Model Of Metabolic Syndrome Lowers Fitness Of High Exercise Capacity Rats (HCR/ Tol ) By Impairing Energy Homeostasis And Increasing Blood Pressure

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Guannan Zhou ◽  
Tao Yang ◽  
Sivarajan Kumarasamy ◽  
Bina Joe ◽  
Lauren G Koch
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Energy Metabolism ◽  
Gut Microbiota ◽  
Exercise Capacity ◽  
Energy Homeostasis ◽  
Current Knowledge ◽  
Strong Predictor ◽  
Whole Body ◽  
Acid Oxidation

Introduction: Low exercise capacity is a strong predictor of cardiovascular disease and overall mortality. Previously we have shown that rats artificially selected for low intrinsic exercise capacity (LCR) have reduced longevity and develop features consistent with metabolic syndrome (MetS) compared to high intrinsic exercise capacity rats (HCR). Current knowledge suggests that gut microbiota is an important contributor for host fitness. Thus, we hypothesized that transferring gut microbiota from LCR rats into inbred high capacity runner (HCR /Tol ) rats would increase risk factors for MetS, including high blood pressure (BP), gain in body weight (BW), and altered resting energy metabolism. Methods: Gut microbiota was depleted in male HCR/ Tol rats (4 mo.) by an antibiotic cocktail given orally (50mg/kg of BW/day) for 5 days, followed by weekly fecal microbiota transfer (FMT) from male LCR or HCR rats (13 mo.) to generate HCR/ Tol -LCR FMT (n = 5) or HCR/ Tol -HCR FMT (n = 6) groups. BW was measured every 4 weeks. At week 11, whole body metabolism was measured by indirect calorimetry (Oxymax, Columbus Instruments). Respiratory Exchange Ratio (RER), Energy Expenditure (EE), glucose and fat oxidation were calculated from oxygen consumption and carbon dioxide release (VO 2 and VCO 2 ). At week 12, BP was measured by tail-cuff method (Kent Scientific) and treadmill exercise test was done at week 13. Results: Compared to HCR/ Tol -HCR FMT , HCR/ Tol -LCR FMT showed a significant gain in BW (7.2% vs 1.9%, P<0.05), elevated systolic BP (147 vs 120 mmHg, P<0.0001), diastolic BP (112 vs 91 mmHg, P<0.01), and mean BP (123 vs 100 mmHg, P<0.001). BP changes in HCR/ Tol -LCR FMT associated with 1) increased VO 2 (355 vs 320 ml/hr, P<0.05), 2) elevated VCO 2 (350 vs 298 ml/hr, P<0.01), 3) increased EE (1.8 vs 1.6 kcal/hr, P<0.01), 4) higher RER (0.96 vs 0.91, P<0.001), 5) higher glucose oxidation (1.36 vs 1.12 g/kg/hr, P<0.001) and 6) reduced fatty acid oxidation (0.09 vs 0.15 g/kg/hr, P<0.01) and a 23% lower exercise capacity. Conclusions: Gut microbiota from LCR rats strongly associated with poor health outcomes, notably elevated BP and impaired energy metabolism. These findings suggest that altered energy homeostasis by microbiota is mechanistically linked to host BP regulation within MetS.

scholarly journals Sleep-wake regulation is altered in leptin-resistant (db/db) genetically obese and diabetic mice

2008 ◽  
Vol 295 (6) ◽  
pp. R2059-R2066 ◽  
Author(s):  
A. D. Laposky ◽  
M. A. Bradley ◽  
D. L. Williams ◽  
J. Bass ◽  
F. W. Turek
Keyword(s):  
Energy Metabolism ◽  
Eye Movement ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Sleep Time ◽  
Rapid Eye Movement ◽  
Sleep Regulation ◽  
Compensatory Response ◽  
Leptin Signaling ◽  
Obesity And Diabetes

Recent epidemiological and clinical studies indicate that the control of sleep-wake states may be an important factor in the regulation of energy metabolism. Leptin is a peripherally synthesized hormone that has critical signaling properties in the brain for the control of long-term energy homeostasis. In this study, we examined the hypothesis that leptin signaling exerts a role in sleep-wake regulation and that leptin may represent an important mechanistic link in the coordination of sleep-wake states and metabolism. Sleep-wake patterns were recorded in a genetic mouse model of obesity and diabetes, the db/db mouse, which harbors a mutation in a particular isoform of the leptin receptor (long form, LRb). We found that db/db mice exhibit a variety of alterations in sleep regulation, including an increase in overall sleep time, a dramatic increase in sleep fragmentation, attenuated diurnal rhythmicity in rapid eye movement sleep and non-rapid eye movement EEG delta power (a measure of sleep homeostatic drive), and a decrease in the compensatory response to acute (i.e., 6 h) sleep deprivation. The db/db mice also generated low amounts of locomotor activity and a reduction in the diurnal rhythm of activity. These results indicate that impaired leptin signaling has deleterious effects on the regulation of sleep amount, sleep architecture, and temporal consolidation of these arousal states. In summary, leptin may represent an important molecular component in the integration of sleep, circadian rhythms, and energy metabolism.

scholarly journals Adipose tissue NAD+ biosynthesis is required for regulating adaptive thermogenesis and whole-body energy homeostasis in mice

2019 ◽  
Vol 116 (47) ◽  
pp. 23822-23828 ◽  
Author(s):  
Shintaro Yamaguchi ◽  
Michael P. Franczyk ◽  
Maria Chondronikola ◽  
Nathan Qi ◽  
Subhadra C. Gunawardana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Lipolytic Activity ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Adaptive Thermogenesis ◽  
Body Energy

Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme for cellular energy metabolism. The aim of the present study was to determine the importance of brown and white adipose tissue (BAT and WAT) NAD+ metabolism in regulating whole-body thermogenesis and energy metabolism. Accordingly, we generated and analyzed adipocyte-specific nicotinamide phosphoribosyltransferase (Nampt) knockout (ANKO) and brown adipocyte-specific Nampt knockout (BANKO) mice because NAMPT is the rate-limiting NAD+ biosynthetic enzyme. We found ANKO mice, which lack NAMPT in both BAT and WAT, had impaired gene programs involved in thermogenesis and mitochondrial function in BAT and a blunted thermogenic (rectal temperature, BAT temperature, and whole-body oxygen consumption) response to acute cold exposure, prolonged fasting, and administration of β-adrenergic agonists (norepinephrine and CL-316243). In addition, the absence of NAMPT in WAT markedly reduced adrenergic-mediated lipolytic activity, likely through inactivation of the NAD+–SIRT1–caveolin-1 axis, which limits an important fuel source fatty acid for BAT thermogenesis. These metabolic abnormalities were rescued by treatment with nicotinamide mononucleotide (NMN), which bypasses the block in NAD+ synthesis induced by NAMPT deficiency. Although BANKO mice, which lack NAMPT in BAT only, had BAT cellular alterations similar to the ANKO mice, BANKO mice had normal thermogenic and lipolytic responses. We also found NAMPT expression in supraclavicular adipose tissue (where human BAT is localized) obtained from human subjects increased during cold exposure, suggesting our finding in rodents could apply to people. These results demonstrate that adipose NAMPT-mediated NAD+ biosynthesis is essential for regulating adaptive thermogenesis, lipolysis, and whole-body energy metabolism.

scholarly journals RBP4: a controversial adipokine

2011 ◽  
Vol 165 (5) ◽  
pp. 703-711 ◽  
Author(s):  
Primoz Kotnik ◽  
Pamela Fischer-Posovszky ◽  
Martin Wabitsch
Keyword(s):  
Insulin Resistance ◽  
Children And Adolescents ◽  
Biologically Active ◽  
Retinol Binding Protein ◽  
Confounding Factors ◽  
Endocrine Organ ◽  
Retinol Binding Protein 4 ◽  
The Metabolic Syndrome

Adipose tissue is an endocrine organ secreting biologically active factors called adipokines that act on both local and distant tissues. Adipokines have an important role in the development of obesity-related comorbidities not only in adults but also in children and adolescents. Retinol binding protein 4 (RBP4) is a recently identified adipokine suggested to link obesity with its comorbidities, especially insulin resistance, type 2 diabetes (T2D), and certain components of the metabolic syndrome. However, data, especially resulting from the clinical studies, are conflicting. In this review, we summarize up-to-date knowledge on RBP4's role in obesity, development of insulin resistance, and T2D. Special attention is given to studies on children and adolescents. We also discuss the role of possible confounding factors that should be taken into account when critically evaluating published studies or planning new studies on this exciting adipokine.

scholarly journals Hepatic JARID1a ablation disrupts the transcription adaptation to feeding and alters systemic metabolism

2018 ◽  
Author(s):  
Kacee A. DiTacchio ◽  
Diana Kalinowska ◽  
Anand Saran ◽  
Ashley Byrne ◽  
Christopher Vollmers ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Circadian Clock ◽  
Lean Body Mass ◽  
Body Mass ◽  
Nutrient Availability ◽  
Energy Homeostasis ◽  
Glucose Production ◽  
Whole Body ◽  
Proper Function ◽  
Hepatic Transcriptome

AbstractThe liver is a key regulator of systemic energy homeostasis whose proper function is dependent on the circadian clock. Here, we show that livers deficient in the oscillator component JARID1a exhibit a dysregulation of genes involved in energy metabolism. Importantly, we find that mice that lack hepatic JARID1a have decreased lean body mass, decreased respiratory exchange ratios, faster production of ketones and increased glucose production in response to fasting. Finally, we find that JARID1a loss compromises the response of the hepatic transcriptome to nutrient availability. In all, ablation of hepatic JARID1a disrupts the coordination of hepatic metabolic programs with whole-body consequences.

Aging Influences the Value of Serum Leptin as Prostate Cancer Risk Factor

2013 ◽  
Vol 09 (01) ◽  
pp. 10 ◽  
Author(s):  
Mauro Bologna ◽  
Patrizia Sanità ◽  
Carlo Vicentini ◽  
Adriano Angelucci ◽  
◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
Risk Factor ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Prostate Cancer Risk ◽  
Visceral Obesity ◽  
Whole Body ◽  
Serum Leptin ◽  
Inflammatory Status

Depository fat functions as endocrine tissue able to regulate whole-body energy homeostasis. Obesity and aging are independently associated with a deregulation of adipose tissue, resulting in pro-inflammatory status and excessive release of adipokines. These events are under investigation for a possible synergism in determining chronic diseases, including cardiovascular illnesses and several types of cancer. Our data, obtained through an observational study conducted with prostate cancer patients, confirmed the association of leptin, an adipose tissue-derived adipokine, with cancer, and suggested that serum leptin represents a stronger risk factor for prostate cancer (PCa) in older than in younger subjects. In elderly patients, visceral obesity measured by waist to hip ratio provided a better correlation with serum leptin in terms of body mass index (BMI) measurements and appeared to be a more adequate indicator for obesity. The expression of leptin receptor mainly observed in invasive prostate carcinoma tissue and in aggressive prostate cancer cell lines suggests a possible molecular link between persistently high leptin levels, seen in aged obese subjects, and PCa progression.

scholarly journals Neuroendocrine Regulation of Energy Metabolism Involving Different Types of Adipose Tissues

2019 ◽  
Vol 20 (11) ◽  
pp. 2707 ◽  
Author(s):  
Qi Zhu ◽  
Bradley J. Glazier ◽  
Benjamin C. Hinkel ◽  
Jingyi Cao ◽  
Lin Liu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Energy Balance ◽  
Energy Homeostasis ◽  
Neural Circuits ◽  
Tissue Imaging ◽  
Whole Body ◽  
Neuroendocrine Regulation ◽  
Positive Energy ◽  
Adipose Tissues ◽  
The Brain

Despite tremendous research efforts to identify regulatory factors that control energy metabolism, the prevalence of obesity has been continuously rising, with nearly 40% of US adults being obese. Interactions between secretory factors from adipose tissues and the nervous system innervating adipose tissues play key roles in maintaining energy metabolism and promoting survival in response to metabolic challenges. It is currently accepted that there are three types of adipose tissues, white (WAT), brown (BAT), and beige (BeAT), all of which play essential roles in maintaining energy homeostasis. WAT mainly stores energy under positive energy balance, while it releases fuels under negative energy balance. Thermogenic BAT and BeAT dissipate energy as heat under cold exposure to maintain body temperature. Adipose tissues require neural and endocrine communication with the brain. A number of WAT adipokines and BAT batokines interact with the neural circuits extending from the brain to cooperatively regulate whole-body lipid metabolism and energy homeostasis. We review neuroanatomical, histological, genetic, and pharmacological studies in neuroendocrine regulation of adipose function, including lipid storage and mobilization of WAT, non-shivering thermogenesis of BAT, and browning of BeAT. Recent whole-tissue imaging and transcriptome analysis of differential gene expression in WAT and BAT yield promising findings to better understand the interaction between secretory factors and neural circuits, which represents a novel opportunity to tackle obesity.

scholarly journals Anti-Obesity Phenotypic Screening Looking to Increase OBR Cell Surface Expression

2013 ◽  
Vol 19 (1) ◽  
pp. 88-99 ◽  
Author(s):  
Tae-Hee Kim ◽  
Dong-Hwa Choi ◽  
Virginie Vauthier ◽  
Julie Dam ◽  
Xiaolan Li ◽  
...  
Keyword(s):  
Cell Surface ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Surface Expression ◽  
Leptin Resistance ◽  
Whole Body ◽  
Cell Surface Expression ◽  
Phenotypic Screening ◽  
Obese People ◽  
Body Energy

The leptin receptor, OBR, is involved in the regulation of whole-body energy homeostasis. Most obese people are resistant to leptin and do not respond to the hormone. The prevention and reversal of leptin resistance is one of the major current goals of obesity research. We showed previously that increased OBR cell surface expression concomitantly increases cellular leptin signaling and prevents obesity development in mice. Improvement of OBR cell surface expression can thus be considered as an interesting anti-obesity therapeutic strategy. To identify compounds that increase the surface expression of OBR, we developed a cell-based, phenotypic assay to perform a high-content screen (HCS) against a library of 50,000 chemical compounds. We identified 67 compounds that increased OBR cell surface expression with AC50 values in the low micromolar range and no effect on total OBR expression and cellular toxicity. Compounds were classified into 16 chemical clusters, of which 4 potentiated leptin-promoted signaling through the JAK2/STAT3 pathway. In conclusion, development of a robust phenotypic screening approach resulted in the discovery of four new scaffolds that demonstrate the desired biological activity and could constitute an original therapeutic solution against obesity and associated disorders.

scholarly journals Disruption of Peripheral Leptin Signaling in Mice Results in Hyperleptinemia without Associated Metabolic Abnormalities

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3987-3997 ◽  
Author(s):  
Kaiying Guo ◽  
Julie E. McMinn ◽  
Thomas Ludwig ◽  
Yi-Hao Yu ◽  
Guoqing Yang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Food Intake ◽  
Leptin Receptor ◽  
Feedback Regulation ◽  
Whole Body ◽  
Negative Feedback Regulation ◽  
Leptin Signaling ◽  
Relative Contribution ◽  
Body Energy

Although central leptin signaling appears to play a major role in the regulation of food intake and energy metabolism, the physiological role of peripheral leptin signaling and its relative contribution to whole-body energy metabolism remain unclear. To address this question, we created a mouse model (Cre-Tam mice) with an intact leptin receptor in the brain but a near-complete deletion of the signaling domain of leptin receptor in liver, adipose tissue, and small intestine using a tamoxifen (Tam)-inducible Cre-LoxP system. Cre-Tam mice developed marked hyperleptinemia (∼4-fold; P &lt; 0.01) associated with 2.3-fold increase (P &lt; 0.05) in posttranscriptional production of leptin. Whereas this is consistent with the disruption of a negative feedback regulation of leptin production in adipose tissue, there were no discernable changes in energy balance, thermoregulation, and insulin sensitivity. Hypothalamic levels of phosphorylated signal transducer and activator of transcription 3, neuropeptide expression, and food intake were not changed despite hyperleptinemia. The percentage of plasma-bound leptin was markedly increased (90.1–96 vs. 41.8–74.7%; P &lt; 0.05), but plasma-free leptin concentrations remained unaltered in Cre-Tam mice. We conclude from these results that 1) the relative contribution to whole-body energy metabolism from peripheral leptin signaling is insignificant in vivo, 2) leptin signaling in adipocyte constitutes a distinct short-loop negative feedback regulation of leptin production that is independent of tissue metabolic status, and 3) perturbation of peripheral leptin signaling alone, although increasing leptin production, may not be sufficient to alter the effective plasma levels of leptin because of the counter-regulatory increase in the level of leptin binding protein(s).

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