Special Issue "Leptin"

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (20 July 2019).

Special Issue Editors

Guest Editor
Prof. Dr. Carlos Diéguez González Website E-Mail
Univ Santiago de Compostela, Inst Invest Sanitaria, CIMUS, Dept Physiol, Santiago De Compostela 15782, Spain
Interests: Endocrinology; growth hormone; leptin; ghrelin; energy metabolism
Co-Guest Editor
Prof. Gema Frühbeck E-Mail
Clin Univ Navarra, Metab Res Lab, Avda Pio 12,36, Pamplona 31008, Spain

Special Issue Information

Dear Colleagues,

From an historical point of view there little doubt that the main scienfic development in the field of obesity was the identification of leptin 25 years ago by J. Friedmann. Among many other things, this discovery allowed : a) the recognition of adipose tissue as the secretory organ, with leptin as one of the main adipokines; b) the understanding of the mechanisms governing the energy balance, with particular emphasis in the actions it exerts at the CNS; c) Newer effects exerted at the central level, including metabolic homeostasis, temperature or reward-related mechanisms; d) understanding the adaptations undertaken by many different endocrine systems (thyroid, gonadal, adrenal) in relation to the energy balance; e) the uncovering of some unexpected roles in the regulation of immune function and inflammatory processes; f) the definition of the diagnosis and genetic basis of some subtypes of human obesity (mutations in the leptin and the leptin receptor gene); and g) the treatment of patients with leptin deficiency, including patients with lipodystrophy.

In this Special Issue we welcome contributions related to any aspect of leptin, from mechanistic issues related to the leptin system, to its biological effects. We aim to provide readers with a clear view of the physiological relevance, the role of leptin in disease states including preclinical models, its diagnostic potential, and the therapeutic implications of the leptin system.

Prof. Carlos Diéguez González
Guest Editor

Manuscript Submission Information

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Keywords

  • Leptin and leptin receptor gene expression.
  • The leptin system and energy balance
  • The leptin system and metabolic homeostasis.
  • Leptin and reward
  • Diet, leptin and neuronal function including neurodegeneration.
  • Leptin and temperature.
  • Leptin and neuroendocrine control of pituitary function (gonadal, adrenal, thyroid, GH).
  • Leptin and cardiovascular function.
  • Leptin, inflammation and the immune system
  • Food deprivation, malnutrition.
  • Leptin in disease states.
  • Leptin-based therapies.

Published Papers (7 papers)

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Research

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Open AccessArticle
Relationships of Trait Anxiety and Loss of Control Eating with Serum Leptin Concentrations among Youth
Nutrients 2019, 11(9), 2198; https://doi.org/10.3390/nu11092198 - 12 Sep 2019
Abstract
Loss of control (LOC) eating in youth is associated with elevated fasting serum leptin, even after accounting for adiposity. Anxiety is closely linked to, and may exacerbate, LOC eating. Yet, it remains unclear how anxiety relates to leptin, or if the relationship is [...] Read more.
Loss of control (LOC) eating in youth is associated with elevated fasting serum leptin, even after accounting for adiposity. Anxiety is closely linked to, and may exacerbate, LOC eating. Yet, it remains unclear how anxiety relates to leptin, or if the relationship is moderated by the presence of LOC eating. We examined whether self-reported trait anxiety interacted with LOC eating in relation to leptin in a convenience sample of youths (n = 592; 13.1 ± 2.7 years; body mass index z-score (BMIz) = 0.9 ± 1.1; 61.8% girls; 53.5% non-Hispanic White; 36.6% with LOC eating). LOC eating was assessed by interview. Leptin was measured after an overnight fast. Exploratory analyses were conducted to examine anxiety and LOC eating in relation to laboratory intake patterns in three sub-samples. In a generalized linear model adjusting for relevant covariates, anxiety significantly interacted with LOC eating in relation to leptin (p = 0.02), such that greater trait anxiety related to higher concentrations of leptin only among youth with LOC eating. Trait anxiety was not significantly related to fasting serum leptin independently in a generalized linear model adjusting for age, race, height, sex, study type, and fat mass (kg). Exploratory mechanistic analyses of food intake patterns did not identify consistent results for participants with both anxiety and LOC eating. Among youth with LOC eating, anxiety may be associated with higher serum leptin. Prospective data are required to elucidate the directionality and mechanisms of these relationships. Full article
(This article belongs to the Special Issue Leptin)
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Open AccessArticle
Hypothalamic–Pituitary and Adipose Tissue Responses to the Effect of Resistin in Sheep: The Integration of Leptin and Resistin Signaling Involving a Suppressor of Cytokine Signaling 3 and the Long Form of the Leptin Receptor
Nutrients 2019, 11(9), 2180; https://doi.org/10.3390/nu11092180 - 11 Sep 2019
Abstract
We hypothesized that resistin is engaged in the development of leptin central insensitivity/resistance in sheep, which is a unique animal model to explore reversible leptin resistance. Thirty Polish Longwool ewes, which were ovariectomized with estrogen replacement, were used. Treatments consisted of the intravenous [...] Read more.
We hypothesized that resistin is engaged in the development of leptin central insensitivity/resistance in sheep, which is a unique animal model to explore reversible leptin resistance. Thirty Polish Longwool ewes, which were ovariectomized with estrogen replacement, were used. Treatments consisted of the intravenous injection of control (saline) or recombinant bovine resistin (rbresistin): control (Control; n = 10), a low dose of rbresistin (R1; 1.0 μg/kg body weight (BW); n = 10), and a high dose of rbresistin (R2; 10.0 μg/kg BW; n = 10). The studies were performed during short-day (SD) and long-day (LD) photoperiods. Leptin and resistin concentrations were determined. Expression levels of a suppressor of cytokine signaling (SOCS)-3 and the long form of the leptin receptor (LeptRb) were determined in selected brain regions, including in the anterior pituitary (AP), hypothalamic arcuate nucleus (ARC), preoptic area (POA), and ventro- and dorsomedial nuclei (VMH/DMH). The results indicate that resistin induced a consistent decrease in LeptRb (except in POA) and an increase in SOCS-3 expression during the LD photoperiod in all selected brain regions. In conclusion, the results demonstrate that the action of resistin appears to be strongly associated with photoperiod-driven changes in the leptin signaling pathway, which may underlie the phenomenon of central leptin resistance. Full article
(This article belongs to the Special Issue Leptin)
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Open AccessArticle
Increase of the Adiponectin/Leptin Ratio in Patients with Obesity and Type 2 Diabetes after Roux-en-Y Gastric Bypass
Nutrients 2019, 11(9), 2069; https://doi.org/10.3390/nu11092069 - 03 Sep 2019
Abstract
Bariatric surgery remains the most effective option for achieving important and sustained weight loss. We explored the effects of Roux-en-Y gastric bypass (RYGB) on the circulating levels of adiponectin, leptin, and the adiponectin/leptin (Adpn/Lep) ratio in patients with obesity and type 2 diabetes [...] Read more.
Bariatric surgery remains the most effective option for achieving important and sustained weight loss. We explored the effects of Roux-en-Y gastric bypass (RYGB) on the circulating levels of adiponectin, leptin, and the adiponectin/leptin (Adpn/Lep) ratio in patients with obesity and type 2 diabetes (T2D). Twenty-five T2D volunteers undergoing RYGB were included in the study, and further subclassified as patients that responded or not to RYBG, regarding remission of T2D. Anthropometric and biochemical variables were evaluated before and after RYGB. Obese patients with T2D exhibited an increase (p < 0.0001) in the Adpn/Lep ratio after RYGB. Changes in the Adpn/Lep ratio correlated better with changes in anthropometric data (p < 0.001) than with the variations of adiponectin or leptin alone. Multiple regression analysis revealed that the change in the Adpn/Lep ratio in patients with T2D was an independent predictor of the changes in body mass index (p < 0.001) and body fat percentage (p = 0.022). However, the Adpn/Lep ratio did not differ between individuals with or without T2D remission after RYGB. In summary, the current study demonstrated that after weight and body fat loss following RYGB, the Adpn/Lep ratio increased in patients with obesity and T2D. Full article
(This article belongs to the Special Issue Leptin)
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Open AccessArticle
Leptin in Human Milk and Child Body Mass Index: Results of the Ulm Birth Cohort Studies
Nutrients 2019, 11(8), 1883; https://doi.org/10.3390/nu11081883 - 13 Aug 2019
Abstract
The objective of the study was to investigate the potential association of human milk leptin concentrations with child body mass index (BMI) and BMI trajectory patterns up to two years of age among children in the Ulm SPATZ Health Study. Leptin concentration was [...] Read more.
The objective of the study was to investigate the potential association of human milk leptin concentrations with child body mass index (BMI) and BMI trajectory patterns up to two years of age among children in the Ulm SPATZ Health Study. Leptin concentration was measured in skimmed human milk by ELISA (R&D System). Child BMI was determined at two to three days, three to four weeks, four to five months, one year, and two years of age. In SPATZ, leptin concentration at six weeks was inversely associated with child BMI at four to five weeks [beta –0.13, 95%CI –0.21;–0.05)] and at three to four months –0.12 –0.21;–0.03)]. Among infants of average BMI shortly after delivery, six week leptin was positively associated with greater increase in BMI from four to five weeks up to two years of age [0.16 (0.04;0.27)]. No associations were observed for six month leptin. Direction of association was the same in the Ulm Birth Cohort Study (UBCS), but statistically insignificant as the point estimate included the null effect value. Our results from SPATZ suggest human milk leptin may play a role in early infant growth. However, it is plausible that the lack of associations in UBCS suggest that these differences of human milk leptin composition between populations could have an impact in infant growth and development in a given population. Full article
(This article belongs to the Special Issue Leptin)
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Open AccessArticle
Adiponectin-leptin Ratio is a Functional Biomarker of Adipose Tissue Inflammation
Nutrients 2019, 11(2), 454; https://doi.org/10.3390/nu11020454 - 22 Feb 2019
Cited by 2
Abstract
Obesity favors the development of cardiometabolic alterations such as type 2 diabetes (T2D) and the metabolic syndrome (MS). Obesity and the MS are distinguished by an increase in circulating leptin concentrations, in parallel to a drop in the levels of adiponectin. Consequently, the [...] Read more.
Obesity favors the development of cardiometabolic alterations such as type 2 diabetes (T2D) and the metabolic syndrome (MS). Obesity and the MS are distinguished by an increase in circulating leptin concentrations, in parallel to a drop in the levels of adiponectin. Consequently, the Adpn/Lep ratio has been suggested as a maker of dysfunctional adipose tissue. We aimed to investigate in humans (n = 292) the reliability of the Adpn/Lep ratio as a biomarker of adipose tissue dysfunction. We considered that an Adpn/Lep ratio of ≥1.0 can be considered normal, a ratio of ≥0.5 <1.0 suggests moderate-medium increased risk, and a ratio of <0.5 indicates a severe increase in cardiometabolic risk. Using these cut-offs, 5%, 54% and 48% of the lean, normoglycemic and without-MS subjects, respectively, fall within the group with an Adpn/Lep ratio below 0.5; while 89%, 86% and 90% of the obese, with T2D and with MS patients fall within the same group (p < 0.001). A significant negative correlation (r = −0.21, p = 0.005) between the Adpn/Lep ratio and serum amyloid A (SAA) concentrations, a marker of adipose tissue dysfunction, was found. We concluded that the Adpn/Lep ratio is a good indicator of a dysfunctional adipose tissue that may be a useful estimator of obesity- and MS-associated cardiometabolic risk, allowing the identification of a higher number of subjects at risk. Full article
(This article belongs to the Special Issue Leptin)
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Review

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Open AccessReview
Functional Relationship between Leptin and Nitric Oxide in Metabolism
Nutrients 2019, 11(9), 2129; https://doi.org/10.3390/nu11092129 - 06 Sep 2019
Abstract
Leptin, the product of the ob gene, was originally described as a satiety factor, playing a crucial role in the control of body weight. Nevertheless, the wide distribution of leptin receptors in peripheral tissues supports that leptin exerts pleiotropic biological effects, consisting of [...] Read more.
Leptin, the product of the ob gene, was originally described as a satiety factor, playing a crucial role in the control of body weight. Nevertheless, the wide distribution of leptin receptors in peripheral tissues supports that leptin exerts pleiotropic biological effects, consisting of the modulation of numerous processes including thermogenesis, reproduction, angiogenesis, hematopoiesis, osteogenesis, neuroendocrine, and immune functions as well as arterial pressure control. Nitric oxide (NO) is a free radical synthesized from L-arginine by the action of the NO synthase (NOS) enzyme. Three NOS isoforms have been identified: the neuronal NOS (nNOS) and endothelial NOS (eNOS) constitutive isoforms, and the inducible NOS (iNOS). NO mediates multiple biological effects in a variety of physiological systems such as energy balance, blood pressure, reproduction, immune response, or reproduction. Leptin and NO on their own participate in multiple common physiological processes, with a functional relationship between both factors having been identified. The present review describes the functional relationship between leptin and NO in different physiological processes. Full article
(This article belongs to the Special Issue Leptin)
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Open AccessReview
Molecular Insight into the Interaction between Epigenetics and Leptin in Metabolic Disorders
Nutrients 2019, 11(8), 1872; https://doi.org/10.3390/nu11081872 - 12 Aug 2019
Abstract
Nowadays, it is well-known that the deregulation of epigenetic machinery is a common biological event leading to the development and progression of metabolic disorders. Moreover, the expression level and actions of leptin, a vast adipocytokine regulating energy metabolism, appear to be strongly associated [...] Read more.
Nowadays, it is well-known that the deregulation of epigenetic machinery is a common biological event leading to the development and progression of metabolic disorders. Moreover, the expression level and actions of leptin, a vast adipocytokine regulating energy metabolism, appear to be strongly associated with epigenetics. Therefore, the aim of this review was to summarize the current knowledge of the epigenetic regulation of leptin as well as the leptin-induced epigenetic modifications in metabolic disorders and associated phenomena. The collected data indicated that the deregulation of leptin expression and secretion that occurs during the course of metabolic diseases is underlain by a variation in the level of promoter methylation, the occurrence of histone modifications, along with miRNA interference. Furthermore, leptin was proven to epigenetically regulate several miRNAs and affect the activity of the histone deacetylases. These epigenetic modifications were observed in obesity, gestational diabetes, metabolic syndrome and concerned various molecular processes like glucose metabolism, insulin sensitivity, liver fibrosis, obesity-related carcinogenesis, adipogenesis or fetal/early postnatal programming. Moreover, the circulating miRNA profiles were associated with the plasma leptin level in metabolic syndrome, and miRNAs were found to be involved in hypothalamic leptin sensitivity. In summary, the evidence suggests that leptin is both a target and a mediator of epigenetic changes that develop in numerous tissues during metabolic disorders. Full article
(This article belongs to the Special Issue Leptin)
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