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Domestic Animal Endocrinology Jul 2016Adiponectin, one of the messenger molecules secreted from adipose tissue that are collectively termed adipokines, has been demonstrated to play a central role in lipid... (Review)
Review
Adiponectin, one of the messenger molecules secreted from adipose tissue that are collectively termed adipokines, has been demonstrated to play a central role in lipid and glucose metabolism in humans and laboratory rodents; it improves insulin sensitivity and exerts antidiabetic and antiinflammatory actions. Adiponectin is synthesized as a 28 kDa monomer but is not secreted as such; instead, it is glycosylated and undergoes multimerization to form different molecular weight multimers before secretion. Adiponectin is one of the most abundant adipokines (μg/mL range) in the circulation. The concentrations are negatively correlated with adipose depot size, in particular with visceral fat mass in humans. Adiponectin exerts its effects by activating a range of different signaling molecules via binding to 2 transmembrane receptors, adiponectin receptor 1 and adiponectin receptor 2. The adiponectin receptor 1 is expressed primarily in the skeletal muscle, whereas adiponectin receptor 2 is predominantly expressed in the liver. Many of the functions of adiponectin are relevant to growth, lactation, and health and are thus of interest in both beef and dairy production systems. Studies on the role of the adiponectin protein in cattle have been impeded by the lack of reliable assays for bovine adiponectin. Although there are species-specific bovine adiponectin assays commercially available, they suffer from a lack of scientific peer-review of validity. Quantitative data about the adiponectin protein in cattle available in the literature emerged only during the last 3 yr and were largely based on Western blotting using either antibodies against human adiponectin or partial peptides from the bovine sequence. Using native bovine high-molecular-weight adiponectin purified from serum, we were able to generate a polyclonal antiserum that can be used for Western blot but also in an ELISA system, which was recently validated. The objective of this review is to provide an overview of the literature about the adiponectin protein in cattle addressing the following aspects: (1) the course of the adiponectin serum concentrations during development in both sexes, during inflammation, nutritional energy deficit and energy surplus, and lactation-induced changes including the response to supplementation with conjugated linoleic acids and with niacin, (2) the concentrations of adiponectin in subcutaneous vs visceral fat depots of dairy cows, (3) the protein expression of adiponectin in tissues other than adipose, and (4) the concentrations in different body fluids including milk.
Topics: Adiponectin; Animals; Body Fluids; Cattle; Female; Male; Sex Factors; Tissue Distribution
PubMed: 27345322
DOI: 10.1016/j.domaniend.2015.11.007 -
Placenta Mar 2021Gestational diabetes mellitus (GDM) is a metabolic syndrome among pregnant mothers that increases the risk of developing growth disorders in the fetus and the placenta....
INTRODUCTION
Gestational diabetes mellitus (GDM) is a metabolic syndrome among pregnant mothers that increases the risk of developing growth disorders in the fetus and the placenta. Adiponectin is an adipokine, which plays a central role in the regulation of glucose and lipid metabolism, energy homeostasis, and insulin resistance in various tissues. Quercetin is a natural flavonoid with beneficial effects in the diabetic animal model, but data related to its effect on histological change and adiponectin system in the placenta of GDM are limited. In the current study, some histological changes and expression of adiponectin and its two receptors in the placenta of rats with GDM were investigated.
METHODS
This study was carried out on placentas from the rodent model. To induce GDM, female rats were treated with a single dose of STZ. Placenta tissue was harvested and stained by PAS method. Protein and mRNA levels of adiponectin and its two receptors were assessed by immunohistochemistry and Real time PCR analysis, respectively.
RESULTS
The results showed the increased number of glycogen cells and thickness of the labyrinth interhemal membrane (LIM) in the embryonic part of the placenta in diabetic rats, while the use of quercetin significantly prevented their increase in diabetic rats. Treatment of the diabetic group with quercetin caused significantly increased adiponectin expression and decreased its receptors.The immunohistochemical study revealed the expression of AdipoR2 in the cytoplasm of syncytiotrophoblast and cytotrophoblast cells.
DISCUSSION
The results indicated that quercetin in pregnant diabetic rats could attenuate the histological abnormalities and improved adiponectin system dysregulation in the placenta.
Topics: Adiponectin; Animals; Diabetes Mellitus, Experimental; Diabetes, Gestational; Female; Male; Placenta; Pregnancy; Quercetin; Rats; Rats, Wistar; Receptors, Adiponectin; Up-Regulation
PubMed: 33640737
DOI: 10.1016/j.placenta.2021.02.008 -
Metabolism: Clinical and Experimental Jan 2020Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this... (Review)
Review
Recent scientific efforts have focused on the detrimental effects that obesity has on the metabolic function of skeletal muscles and whether exercise can improve this dysfunction. In this regard, adiponectin, with important metabolic functions (e.g. insulin-sensitizer and anti-inflammatory), has been recently described as a myokine that acts in an autocrine/paracrine manner. Earlier studies reported that muscle adiponectin could be induced by pro-inflammatory mediators (e.g. lipopolysaccharide), cytokines, and high-fat diets, providing a protective mechanism of this tissue against metabolic insults. However, when metabolic insults such as high-fat diets are sustained this protective response becomes dysregulated, making the skeletal muscle susceptible to metabolic impairments. Recent studies have suggested that exercise could prevent or even reverse this process. Considering that most scientific knowledge on adiponectin dysregulation in obesity is from the study of adipose tissue, the present review summarizes and discusses the literature available to date regarding the effects of obesity on skeletal muscle adiponectin induction, along with the potential effects of different exercise prescriptions on this response in an obesity context.
Topics: Adiponectin; Animals; Exercise; Humans; Insulin Resistance; Muscle, Skeletal; Obesity; Up-Regulation
PubMed: 31706980
DOI: 10.1016/j.metabol.2019.154008 -
Biochemical and Biophysical Research... Jul 2024Ocular inflammation-associated diseases are leading causes of global visual impairment, with limited treatment options. Adiponectin, a hormone primarily secreted by... (Review)
Review
Ocular inflammation-associated diseases are leading causes of global visual impairment, with limited treatment options. Adiponectin, a hormone primarily secreted by adipose tissue, binds to its receptors, which are widely distributed throughout the body, exerting powerful physiological regulatory effects. The protective role of adiponectin in various inflammatory diseases has gained increasing attention in recent years. Previous studies have confirmed the presence of adiponectin and its receptors in the eyes. Furthermore, adiponectin and its analogs have shown potential as novel drugs for the treatment of inflammatory eye diseases. This article summarizes the evidence for the interplay between adiponectin and inflammatory eye diseases and provides new perspectives on the diagnostic and therapeutic possibilities of adiponectin.
Topics: Humans; Adiponectin; Receptors, Adiponectin; Signal Transduction; Animals; Inflammation; Eye Diseases
PubMed: 38710142
DOI: 10.1016/j.bbrc.2024.150041 -
International Journal of Molecular... Jun 2019Adipose tissue has been recognized as a complex organ with endocrine and metabolic roles. The excess of fat mass, as occurs during overweight and obesity states, alters... (Review)
Review
Adipose tissue has been recognized as a complex organ with endocrine and metabolic roles. The excess of fat mass, as occurs during overweight and obesity states, alters the regulation of adipose tissue, contributing to the development of obesity-related disorders. In this regard, many epidemiological studies shown an association between obesity and numerous types of malignancies, comprising those linked to the endocrine system (e.g., breast, endometrial, ovarian, thyroid and prostate cancers). Multiple factors may contribute to this phenomenon, such as hyperinsulinemia, dyslipidemia, oxidative stress, inflammation, abnormal adipokines secretion and metabolism. Among adipokines, growing interest has been placed in recent years on adiponectin (APN) and on its role in carcinogenesis. APN is secreted by adipose tissue and exerts both anti-inflammatory and anti-proliferative actions. It has been demonstrated that APN is drastically decreased in obese individuals and that it can play a crucial role in tumor growth. Although literature data on the impact of APN on carcinogenesis are sometimes conflicting, the most accredited hypothesis is that it has a protective action, preventing cancer development and progression. The aim of the present review is to summarize the currently available evidence on the involvement of APN and its signaling in the etiology of cancer, focusing on endocrine malignancies.
Topics: Adiponectin; Adipose Tissue; Animals; Biomarkers; Cell Transformation, Neoplastic; Endocrine Gland Neoplasms; Humans; Insulin; Models, Biological; Neoplasm Metastasis; Obesity; Paracrine Communication; Protein Binding; Receptors, Adiponectin; Risk; Risk Assessment; Structure-Activity Relationship
PubMed: 31212761
DOI: 10.3390/ijms20122863 -
Neuroscience Letters Jun 2023Adiponectin is a member of the adipokine family and contributes to regulating energy homeostasis, reproduction, and various biological functions, such as insulin...
BACKGROUND & AIM
Adiponectin is a member of the adipokine family and contributes to regulating energy homeostasis, reproduction, and various biological functions, such as insulin receptor signaling pathway sensitivity, mitochondrial biogenesis, oxidative metabolism, neurogenesis, and suppression of inflammation. This study aimed to investigate the effects of intracerebroventricular (ICV) injection of adiponectin and its interaction with the neuropeptide Y (NPY) and GABAergic systems on central appetite regulation in neonatal layer-type chickens.
MATERIALS & METHODS
In this study, 6 experiments were conducted, each of which included 4 experimental groups. In the first experiment, the chickens were injected with saline and adiponectin (20.73, 41.45, and 62.18 nmol). In the second experiment, saline, adiponectin (62.18 nmol), B5063 (NPY1 receptor antagonist, 2.12 nmol), and simultaneous injections of adiponectin and B5063 were performed. Experiments 3 to 6 were done in the same way to experiment 1, but the chickens were injected with SF22 (NPY2 receptor antagonist, 2.66 nmol), SML0891 (NPY5 receptor antagonist, 2.89 nmol), picrotoxin (GABAA receptor antagonist, 0.89 nmol), CGP54626 (GABAB receptor antagonist, 0.047 nmol) instead of B5063. Feed consumption was measured 120 min after the injection.
RESULTS
A dose-dependent increase in appetite was observed after the injection of adiponectin (20.73, 41.45, and 62.18 nmol) (P < 0.05). The injection of B5063 + adiponectin attenuated the hyperphagic effect of adiponectin (P < 0.05). In addition, co-injection of picrotoxin and adiponectin significantly decreased adiponectin-induced hyperphagia (P < 0.05). In addition, adiponectin significantly increased the number of steps, jumps, exploratory food, pecks, and standing time, while decreasing sitting time and rest time (P < 0.05).
CONCLUSION
These results suggest that the hyperphagic effects of adiponectin are probably mediated through NPY1 and GABAA receptors in neonatal layer-type chickens.
Topics: Animals; Adiponectin; Chickens; Eating; Feeding Behavior; Injections, Intraventricular; Neuropeptide Y; Picrotoxin
PubMed: 37142113
DOI: 10.1016/j.neulet.2023.137283 -
American Journal of Physiology. Cell... Mar 2023Vasoactive peptides often serve a multitude of functions aside from their direct effects on vasodynamics. This article will review the existing literature on two... (Review)
Review
Vasoactive peptides often serve a multitude of functions aside from their direct effects on vasodynamics. This article will review the existing literature on two vasoactive peptides and their involvement in skin homeostasis: adiponectin and-as the main representative of the kallikrein-kinin system-bradykinin. Adiponectin is the most abundantly expressed adipokine in the human organism, where it is mainly localized in fat depots including subcutaneous adipose tissue, from where adiponectin can exert paracrine effects. The involvement of adiponectin in skin homeostasis is supported by a number of studies reporting the effects of adiponectin in isolated human keratinocytes, sebocytes, fibroblasts, melanocytes, and immune cells. Regarding skin pathology, the potential involvement of adiponectin in psoriasis, atopic dermatitis, scleroderma, keloid, and melanogenesis is discussed in this article. The kallikrein-kinin system is composed of a variety of enzymes and peptides, most of which have been identified to be expressed in the skin. This also includes the expression of bradykinin receptors on most skin cells. Bradykinin is one of the very few hormones that is targeted by treatment in routine clinical use in dermatology-in this case for the treatment of hereditary angioedema. The potential involvement of bradykinin in wound healing, psoriasis, and melanoma is further discussed in this article. This review concludes with a call for additional preclinical and clinical studies to further explore the therapeutic potential of adiponectin supplementation (for psoriasis, atopic dermatitis, wound healing, scleroderma, and keloid) or pharmacological interference with the kallikrein-kinin system (for wound healing, psoriasis, and melanoma).
Topics: Homeostasis; Adiponectin; Kallikrein-Kinin System; Bradykinin; Humans; Skin Physiological Phenomena; Skin Diseases
PubMed: 36745527
DOI: 10.1152/ajpcell.00269.2022 -
Rheumatology International Sep 2019The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of the IgG and/or IgM isotypes of the antiphospholipid antibodies, thrombosis... (Review)
Review
The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of the IgG and/or IgM isotypes of the antiphospholipid antibodies, thrombosis and/or recurrent pregnancy losses. Various markers of inflammation are associated with clinical and/or laboratory features of APS. Adiponectin (Ad) is a member of the adipocytokines that exert its roles by binding to its receptors (AdR). Peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonists induced Ad production. The aged Pparg null-mice represented the first animal model that spontaneously develops APS and this model emphasized the importance of PPAR-gamma signaling in the development of APS. Recombinant Ad (rAd) application was beneficial for the improvement of glucose, insulin and lipid levels in mice. Orally active AdR agonist exerted similar effects to Ad in mice. Due to the re-occurrence of thrombotic episodes in APS patients (despite life-long anticoagulation), administration of PPAR-gamma agonists, rAd, or AdR agonists should be further tested in experimental models of APS, which eventually, will provide more data for novel therapeutic strategies that will ameliorate clinical manifestations of the APS.
Topics: Adiponectin; Animals; Anti-Inflammatory Agents; Anticoagulants; Antiphospholipid Syndrome; Blood Coagulation; Disease Models, Animal; Humans; Mice, Knockout; PPAR gamma; Receptors, Adiponectin; Signal Transduction
PubMed: 31214769
DOI: 10.1007/s00296-019-04349-x -
Canadian Journal of Diabetes Jun 2017The roles of deficient or deranged insulin, adiponectin and 25 hydroxy vitamin D (25[OH]D) levels regulating food intake, energy metabolism, glucose and lipid metabolism...
OBJECTIVES
The roles of deficient or deranged insulin, adiponectin and 25 hydroxy vitamin D (25[OH]D) levels regulating food intake, energy metabolism, glucose and lipid metabolism and body weight have been reported in the pathogenesis of prediabetes and type 2 diabetes mellitus. However, their congruity in the etiology of diabetes mellitus is unknown. Thus, the aim of the study was to investigate the roles of these parameters together and to establish their interrelationship in patients with prediabetes and diabetes.
METHODS
The preliminary cross-sectional study included 77 persons with type 2 diabetes who were matched for age, sex and body mass index (BMI); 73 persons with prediabetes; and 52 healthy control subjects. Fasting serum levels of adiponectin, insulin and 25(OH)D were measured by commercially available immune assay kits, and routine biochemical parameters were analyzed in all study groups.
RESULTS
The results show statistically significant lower levels of serum adiponectin and serum 25(OH)D and higher serum insulin levels in persons with prediabetes or type 2 diabetes with respect to controls. The changes in the serum adiponectin or serum 25(OH)D in persons with prediabetes and type 2 diabetes were found to be inversely correlated with the serum levels of insulin. Moreover, multiple linear regression analysis, with 25(OH)D, insulin and homeostatic model assessment-insulin resistance (HOMA-IR) as the variables, revealed that serum adiponectin levels might be an independent risk factor for the progression of prediabetes and type 2 diabetes in subjects.
CONCLUSIONS
The association of these hormones might act as a significant predictor of progression of prediabetes to type 2 diabetes. Decreased serum adiponectin levels might be an independent risk factor for progression to prediabetes and type 2 diabetes, which may help in developing experimental models of the disease or in identifying biomarkers or disease-modifying drugs.
Topics: Adiponectin; Adult; Biomarkers; Cross-Sectional Studies; Diabetes Mellitus, Type 2; Female; Humans; Male; Middle Aged; Prediabetic State; Vitamin D
PubMed: 28236525
DOI: 10.1016/j.jcjd.2016.10.006 -
The Journal of Headache and Pain Aug 2023Adipokines, including adiponectin, are implicated in nociceptive pain; however, the underlying cellular and molecular mechanisms remain unknown.
BACKGROUND
Adipokines, including adiponectin, are implicated in nociceptive pain; however, the underlying cellular and molecular mechanisms remain unknown.
METHODS
Using electrophysiological recording, immunostaining, molecular biological approaches and animal behaviour tests, we elucidated a pivotal role of adiponectin in regulating membrane excitability and pain sensitivity by manipulating Cav3.2 channels in trigeminal ganglion (TG) neurons.
RESULTS
Adiponectin enhanced T-type Ca channel currents (I) in TG neurons through the activation of adiponectin receptor 1 (adipoR1) but independently of heterotrimeric G protein-mediated signaling. Coimmunoprecipitation revealed a physical association between AdipoR1 and casein kinase II alpha-subunits (CK2α) in the TG, and inhibiting CK2 activity by chemical inhibitor or siRNA targeting CK2α prevented the adiponectin-induced I response. Adiponectin significantly activated protein kinase C (PKC), and this effect was abrogated by CK2α knockdown. Adiponectin increased the membrane abundance of PKC beta1 (PKCβ1). Blocking PKCβ1 pharmacologically or genetically abrogated the adiponectin-induced I increase. In heterologous expression systems, activation of adipoR1 induced a selective enhancement of Cav3.2 channel currents, dependent on PKCβ1 signaling. Functionally, adiponectin increased TG neuronal excitability and induced mechanical pain hypersensitivity, both attenuated by T-type channel blockade. In a trigeminal neuralgia model induced by chronic constriction injury of infraorbital nerve, blockade of adipoR1 signaling suppressed mechanical allodynia, which was prevented by silencing Cav3.2.
CONCLUSION
Our study elucidates a novel signaling cascade wherein adiponectin stimulates TG Cav3.2 channels via adipoR1 coupled to a novel CK2α-dependent PKCβ1. This process induces neuronal hyperexcitability and pain hypersensitivity. Insight into adipoR-Cav3.2 signaling in sensory neurons provides attractive targets for pain treatment.
Topics: Animals; Mice; Adiponectin; Neurons; Nociception; Pain; Receptors, Adiponectin; Trigeminal Ganglion; Calcium Channels, T-Type
PubMed: 37620777
DOI: 10.1186/s10194-023-01658-2