Reduced Adiponectin Levels Research Articles

Adiponectin Prevents Skin Inflammation in Rosacea by Suppressing S6 Phosphorylation in Keratinocytes

Numerous recent evidence highlights epidemiological connections between rosacea and metabolic disorders. However, the precise path through which metabolic factors impact rosacea risk is still unclear. Therefore, this study aims to investigate the role of adiponectin, a crucial adipokine that regulates metabolic homeostasis, in the pathogenesis of rosacea. We elucidated a detrimental feedback loop between rosacea-like skin inflammation and decreased levels of skin adiponectin. To elaborate, rosacea lesional skin exhibits diminished adiponectin expression compared to non-lesional areas in the same patients. Induction of rosacea-like inflammation reduced adiponectin levels in the skin by generating inflammatory cytokines that suppress adiponectin production from subcutaneous adipocytes. Conversely, complete depletion of adiponectin exacerbated rosacea-like features in the mouse model. Mechanistically, adiponectin deficiency led to heightened S6 phosphorylation, a marker of the mTORC1 signaling pathway, in the epidermis. Adiponectin significantly inhibited S6 phosphorylation in cultured keratinocytes. Notably, replenishing adiponectin whole protein or topically applying an agonist for adiponectin receptor 1 successfully improved rosacea-like features in mice. This study contributes to understanding the role of adiponectin in skin inflammation associated with rosacea pathophysiology, suggesting that restoring adiponectin function in the skin could be a potential therapeutic strategy.

Research progress in biosensors for adiponectin

Adiponectin, a cytokine associated with adipose tissue, is a recently defined adipocytokine involved in insulin, glucose, and adipocyte metabolism. Reduced adiponectin levels can increase the risk of developing metabolic syndrome (MS). Adiponectin is considered an important target for the treatment of type 2 diabetes mellitus (T2DM) and MS due to its anti-atherosclerotic and insulin-sensitizing effects. Therefore, the accurate determination of adiponectin concentrations in human plasma is necessary for the management of both T2DM and MS. A variety of biosensors have been developed for the detection of biomarkers such as adiponectin. This paper reviews the applications of electrochemical sensors, surface-enhanced Raman scattering sensors, and microfluidic chip-based chemiluminescence sensors in the detection of adiponectin and the recent research progress in the sensors for the detection of adiponectin, aiming to provide a reference for the research and application of sensors for adiponectin in the medical field.

Transgenic human C-reactive protein affects oxidative stress but not inflammation biomarkers in the aorta of spontaneously hypertensive rats

BackgroundC-reactive protein (CRP) is an acute inflammatory protein detected in obese patients with metabolic syndrome. Moreover, increased CRP levels have been linked with atherosclerotic disease, congestive heart failure, and ischemic heart disease, suggesting that it is not only a biomarker but also plays an active role in the pathophysiology of cardiovascular diseases. Since endothelial dysfunction plays an essential role in various cardiovascular pathologies and is characterized by increased expression of cell adhesion molecules and inflammatory markers, we aimed to detect specific markers of endothelial dysfunction, inflammation, and oxidative stress in spontaneously hypertensive rats (SHR) expressing human CRP. This model is genetically predisposed to the development of the metabolic syndrome.MethodsTransgenic SHR male rats (SHR-CRP) and non-transgenic SHR (SHR) at the age of 8 months were used. Metabolic profile (including serum and tissue triglyceride (TAG), serum insulin concentrations, insulin-stimulated incorporation of glucose, and serum non-esterified fatty acids (NEFA) levels) was measured. In addition, human serum CRP, MCP-1 (monocyte chemoattractant protein-1), and adiponectin were evaluated by means of ELISA, histological analysis was used to study morphological changes in the aorta, and western blot analysis of aortic tissue was performed to detect expression of endothelial, inflammatory, and oxidative stress markers.ResultsThe presence of human CRP was associated with significantly decreased insulin-stimulated glycogenesis in skeletal muscle, increased muscle and hepatic accumulation of TAG and decreased plasmatic cGMP concentrations, reduced adiponectin levels, and increased monocyte chemoattractant protein-1 (MCP-1) levels in the blood, suggesting pro-inflammatory and presence of multiple features of metabolic syndrome in SHR-CRP animals. Histological analysis of aortic sections did not reveal any visible morphological changes in animals from both SHR and SHR-CRP rats. Western blot analysis of the expression of proteins related to the proper function of endothelium demonstrated significant differences in the expression of p-eNOS/eNOS in the aorta, although endoglin (ENG) protein expression remained unaffected. In addition, the presence of human CRP in SHR in this study did not affect the expression of inflammatory markers, namely p-NFkB, P-selectin, and COX2 in the aorta. On the other hand, biomarkers related to oxidative stress, such as HO-1 and SOD3, were significantly changed, indicating the induction of oxidative stress.ConclusionsOur findings demonstrate that CRP alone cannot fully induce the expression of endothelial dysfunction biomarkers, suggesting other risk factors of cardiovascular disorders are necessary to be involved to induce endothelial dysfunction with CRP.

The role of adipokines and ghrelin in interactions and clinical implications in childhood obesity.

Childhood obesity is a growing global health concern, especially prevalent in the Arabian Peninsula, and is known to contribute to metabolic syndrome and insulin resistance. This study aimed to investigate the interplay between adipokines (leptin and adiponectin), ghrelin, and insulin homeostasis in childhood obesity. A case-control study was conducted in Babylon involving 120 children/adolescents (7-17 years). The participants were divided into two groups: 60 obese and 60 healthy controls. Anthropometric and biochemical measures were examined, applying World Health Organization (WHO) growth standards to categorize weight status. Data on blood lipids, glucose, adipokines, and ghrelin were collected in Babylon (Merjan Medical City), ensuring accuracy and providing insights into pediatric obesity's metabolic and hormonal status. Clinical, anthropometric, and laboratory attributes of children were evaluated, with classification as normal-weight or obese based on BMI/Z-score and Waist Circumference. The obese group exhibited elevated triglycerides and insulin levels, as well as reduced adiponectin levels (P ≤ 0.001). Leptin levels showed a positive correlation with BMI/Z-score (r = 0.352, P = 0.006). A diagnostic model demonstrated the significant diagnostic capacity of leptin (AUC > 99%) and its importance in predicting childhood obesity. Each unit increase in leptin elevated the probability of obesity by a factor of 1.197 (95% CI: 1.0507-1.3632, P = 0.0068). The study revealed significant differences in clinical, biochemical, and biological markers of obesity between the research groups and the control group. Leptin emerged as a significant predictor of obesity, demonstrating high diagnostic accuracy. The complex interactions among these adipokines underscore the necessity for comprehensive obesity management strategies.

Altered Red Blood Cell Fatty Acid and Serum Adipokine Profiles in Subjects with Obesity.

Adipokines, as well as the fatty acid profile of red blood cell (RBC) membranes, are known to play important roles in the development and progression of metabolic complications induced by obesity. Thus, the objective of this study is to compare the serum adipokine profile and the RBC membrane fatty acid profile of normal-weight and obese adults, and to analyze their relationship with serum biochemical parameters. An observational case-control study was performed in 75 normal-weight and obese adult subjects. Biochemical serum parameters, eight serum adipokines and the RBC membrane fatty acid profiles were measured. Associations between parameters were established using regression analysis. Subjects with obesity showed increased levels of leptin, fibroblast growth factor 21 (FGF21) and overexpressed nephroblastoma (NOV/CCN3), decreased adiponectin, and similar levels of vaspin and chemerin compared to normal-weight subjects. Significant positive and negative correlations were found with triglycerides and high-density lipoprotein-cholesterol (HDL-c), respectively. An increase in the total ω-6 fatty acids in the RBC membrane fatty acid profiles in subjects with obesity was observed, because of higher levels of both dihomo-γ-linolenic acid (DGLA) and arachidonic acid (AA), and decreased total ω-3 fatty acids, mainly due to lower levels of docosahexaenoic acid (DHA). The ω-6/ω-3 ratio in the RBCs was significantly higher, suggesting an inflammatory status, as was also suggested by a reduced adiponectin level. A negative association between DGLA and adiponectin, and a positive association between DHA and serum triglycerides, was observed. Important alterations in serum adipokine and RBC fatty acid profiles are found in subjects with obesity.

Adiponectin stimulates Sca1+CD34−-adipocyte precursor cells associated with hyperplastic expansion and beiging of brown and white adipose tissue

BackgroundThe adipocyte hormone adiponectin improves insulin sensitivity and there is an inverse correlation between adiponectin levels and type-2 diabetes risk. Previous research shows that adiponectin remodels the adipose tissue into a more efficient metabolic sink. For instance, mice that overexpress adiponectin show increased capacity for hyperplastic adipose tissue expansion as evident from smaller and metabolically more active white adipocytes. In contrast, the brown adipose tissue (BAT) of these mice looks “whiter” possibly indicating reduced metabolic activity. Here, we aimed to further establish the effect of adiponectin on adipose tissue expansion and adipocyte mitochondrial function as well as to unravel mechanistic aspects in this area. MethodsBrown and white adipose tissues from adiponectin overexpressing (APN tg) mice and littermate wildtype controls, housed at room and cold temperature, were studied by histological, gene/protein expression and flow cytometry analyses. Metabolic and mitochondrial functions were studied by radiotracers and Seahorse-based technology. In addition, mitochondrial function was assessed in cultured adiponectin deficient adipocytes from APN knockout and heterozygote mice. ResultsAPN tg BAT displayed increased proliferation prenatally leading to enlarged BAT. Postnatally, APN tg BAT turned whiter than control BAT, confirming previous reports. Furthermore, elevated adiponectin augmented the sympathetic innervation/activation within adipose tissue. APN tg BAT displayed reduced metabolic activity and reduced mitochondrial oxygen consumption rate (OCR). In contrast, APN tg inguinal white adipose tissue (IWAT) displayed enhanced metabolic activity. These metabolic differences between genotypes were apparent also in cultured adipocytes differentiated from BAT and IWAT stroma vascular fraction, and the OCR was reduced in both brown and white APN heterozygote adipocytes. In both APN tg BAT and IWAT, the mesenchymal stem cell-related genes were upregulated along with an increased abundance of Lineage−Sca1+CD34− “beige-like” adipocyte precursor cells. In vitro, the adiponectin receptor agonist Adiporon increased the expression of the proliferation marker Pcna and decreased the expression of Cd34 in Sca1+ mesenchymal stem cells. ConclusionsWe propose that the seemingly opposite effect of adiponectin on BAT and IWAT is mediated by a common mechanism; while reduced adiponectin levels are linked to lower adipocyte OCR, elevated adiponectin levels stimulate expansion of adipocyte precursor cells that produce adipocytes with intrinsically higher metabolic rate than classical white but lower metabolic rate than classical brown adipocytes. Moreover, adiponectin can modify the adipocytes' metabolic activity directly and by enhancing the sympathetic innervation within a fat depot.

Multifactorial Aspects of Adiponectin in Non- Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a significant worldwide health issue strongly associated with obesity and metabolic syndrome. It underscores the critical role of adiponectin, a significant adipokine, in the disease's intricate progression. NAFLD's complexity stems from its interplay with factors like obesity, diabetes, and metabolic syndrome, with reduced adiponectin levels commonly observed in NAFLD patients, influenced by age, gender, lipid profiles, and insulin resistance. Adiponectin's versatility in mitigating insulin resistance, inflammation, and liver fibrosis makes it a focal point in NAFLD research, while recent studies introduce spexin, a neuropeptide, as a potential correlate, adding to the understanding of metabolic disorders. To tailor treatment approaches, recognizing the factors affecting adiponectin levels, such as genetics, lifestyle, and comorbidities, is crucial. Lifestyle changes and specific medications offer promise in improving NAFLD outcomes by modulating adiponectin. The article underscores adiponectin's central role in the complex NAFLD landscape and the need for further research to fully grasp its mechanisms and therapeutic potential in managing this prevalent liver disease, emphasizing the importance of rebalancing adipokines and enhancing metabolic health.

The role of adiponectin in gastric cancer

Adiponectin, an adipokine synthesized by adipose tissue, has garnered significant attention in biomedical investigations. Research on its implications suggests that reduced adiponectin levels in the bloodstream might serve as a potential predisposing factor for several types of cancers, including gastric cancer. Although many studies on adiponectin levels in gastric cancer patients have been reported, its predictive role as a biomarker remains controversial. Moreover, the significance of adiponectin receptor expression as a prognostic factor in gastric cancer tissues varies across different research studies, and the precise mechanism by which adiponectin influences the initiation and advancement of gastric cancer remains to be fully elucidated. Furthermore, the anti-inflammatory and postoperative anti-infective effects of adiponectin are worth further investigation. Based on existing studies, it is commonly suggested that in the presence of low adiponectin levels, the stomach might be vulnerable to stimulation or damage from certain carcinogens, promoting gastric cancer development and progression. Considering its complex systemic effects and high serum concentration, adiponectin might serve as a homeostasis regulator and not necessarily as an anti-cancer factor. In this review, we explore the current research available on adiponectin in relation to gastric cancer and discuss its role and corresponding receptors involved in gastric cancer.

Molecular Study on Single Nucleotide Polymorphism of Adiponectin Gene and its Association with Type II Diabetes in Egyptian Patients

Background: Type 2 diabetes mellitus is a prevalent hereditary condition that has multiple genetic risk factors as well as environmental influences. Aim: The Work aimed to find if there is an association between the presence of Single Nucleotide Polymorphism of the Adiponectin gene & its association with type II diabetes in Egyptian patients. Material & Techniques: This case-control research had been conducted at Molecular Biology and Biochemistry, Genetic Engineering & biotechnology institute, university of Sadat city. This research had been conducted on eighty patients; separated into 2 groups diabetic group and the control group. Results: significant reduction in adiponectin level in type II diabetes studied cases compared to normal control subjects (p <0.001). GG genotype is significantly more predominant in type 2 diabetes (54%) while the GT genotype is more predominant in control (60%) (p-value =0.04)., while no variation in allele distribution among both groups (p value=0.6). Conclusion: In studied cases with type 2 diabetes, there was a significant reduction in adiponectin levels in type II diabetes patients. GG genotype is significantly more predominant in type 2 diabetes. The genotype GG significantly rises the risk of occurrence of type 2 diabetes.

Cucumeropsis mannii seed oil ameliorates Bisphenol-A-induced adipokines dysfunctions and dyslipidemia.

This study demonstrated the therapeutic potentials of Cucumeropsis mannii seed oil (CMSO) capable of alleviating BPA-induced dyslipidemia and adipokine dysfunction. In this study, we evaluated the effects of CMSO on adipokine dysfunctions and dyslipidemia in bisphenol-A (BPA)-induced male Wistar rats. Six-week-old 36 albino rats of 100-200 g weight were assigned randomly to six groups, which received varied doses of BPA and/or CMSO. The administration of BPA and CMSO was done at the same time for 42 days by oral intubation. The adipokine levels and lipid profile were measured in adipose tissue and plasma using standard methods. BPA induced significant (p < .05) increases in triglycerides, cholesterol, leptin, LDL-C, and atherogenic and coronary risk indices in adipose tissue and plasma, as well as a decrease in adiponectin and HDL-C levels in Group II animals. BPA administration significantly (p < .05) elevated Leptin levels and reduced adiponectin levels. BPA plus CMSO reduced triglycerides, cholesterol, leptin, LDL-C, and atherogenic and coronary risk indices while increasing adiponectin levels and HDL-C in adipose tissue and plasma (p < .05). The results showed that BPA exposure increased adipose tissue as well as serum levels of the atherogenic index, triglycerides, cholesterol, coronary risk index, LDL-C, leptin, and body weight with decreased adiponectin levels and HDL-C. Treatment with CMSO reduced the toxicities caused by BPA in rats by modulating the body weight, adiponectin/leptin levels, and lipid profiles in serum and adipose tissue. This study has shown that CMSO ameliorates BPA-induced dyslipidemia and adipokine dysfunctions. We suggest for further clinical trial to establish the clinical applications.

Aerobic physical training impact on adipokines in women with polycystic ovary syndrome - Effects of body fat percentage.

We investigated the effects of aerobic training on adipokine concentrations in women with polycystic ovary syndrome (PCOS). 120 women, including 60 with PCOS and 60 without PCOS, were divided into six groups (n = 20) based on body fat percentages of 22%-27%, 28%-32%, and 33%-37%. All groups were submitted the same evaluations before and after 16 weeks of aerobic training. These included anthropometric and hemodynamic analyses, cardiopulmonary tests, and laboratory tests. Two-way analysis of variance was performed to evaluate the differences between women with and without PCOS, effect of the body fat percentage, and effect of aerobic training. Body fat and PCOS were associated with high values of blood glucose, insulin, and testosterone. Body fat also reduced adiponectin levels and increased leptin, tumor necrosis factoralpha (TNF-α), and interleukin-6 (IL-6). In contrast, the PCOS increased only TNF-α and IL-6 levels. In the PCOS group, aerobic training reduced insulin, triglycerides, leptin, and IL-6 levels. It also promoted an increase in adiponectin and high-density lipoprotein levels. However, aerobic training did not alter TNF-α concentrations. The body fat potentiates metabolic impairments that may be harmful to women with PCOS. Aerobic training appears to promote an important beneficial effect on the metabolic regulation of adipokines, except TNF-α.

Adipocyte-specific ablation of the Ca2+ pump SERCA2 impairs whole-body metabolic function and reveals the diverse metabolic flexibility of white and brown adipose tissue

ObjectiveSarco/endoplasmic reticulum Ca2+-ATPase (SERCA) transports Ca2+ from the cytosol into the endoplasmic retitculum (ER) and is essential for appropriate regulation of intracellular Ca2+ homeostasis. The objective of this study was to test the hypothesis that SERCA pumps are involved in the regulation of white adipocyte hormone secretion and other aspects of adipose tissue function and that this control is disturbed in obesity-induced type-2 diabetes. MethodsSERCA expression was measured in isolated human and mouse adipocytes as well as in whole mouse adipose tissue by Western blot and RT-qPCR. To test the significance of SERCA2 in adipocyte functionality and whole-body metabolism, we generated adipocyte-specific SERCA2 knockout mice. The mice were metabolically phenotyped by glucose tolerance and tracer studies, histological analyses, measurements of glucose-stimulated insulin release in isolated islets, and gene/protein expression analyses. We also tested the effect of pharmacological SERCA inhibition and genetic SERCA2 ablation in cultured adipocytes. Intracellular and mitochondrial Ca2+ levels were recorded with dual-wavelength ratio imaging and mitochondrial function was assessed by Seahorse technology. ResultsWe demonstrate that SERCA2 is downregulated in white adipocytes from patients with obesity and type-2 diabetes as well as in adipocytes from diet-induced obese mice. SERCA2-ablated adipocytes display disturbed Ca2+ homeostasis associated with upregulated ER stress markers and impaired hormone release. These adipocyte alterations are linked to mild lipodystrophy, reduced adiponectin levels, and impaired glucose tolerance. Interestingly, adipocyte-specific SERCA2 ablation leads to increased glucose uptake in white adipose tissue while the glucose uptake is reduced in brown adipose tissue. This dichotomous effect on glucose uptake is due to differently regulated mitochondrial function. In white adipocytes, SERCA2 deficiency triggers an adaptive increase in fibroblast growth factor 21 (FGF21), increased mitochondrial uncoupling protein 1 (UCP1) levels, and increased oxygen consumption rate (OCR). In contrast, brown SERCA2 null adipocytes display reduced OCR despite increased mitochondrial content and UCP1 levels compared to wild type controls. ConclusionsOur data suggest causal links between reduced white adipocyte SERCA2 levels, deranged adipocyte Ca2+ homeostasis, adipose tissue dysfunction and type-2 diabetes.

Adiponectin Deficiency Alters Placenta Function but Does Not Affect Fetal Growth in Mice.

Adiponectin administration to pregnant mice decreases nutrient transport and fetal growth. An adiponectin deficiency, on the other hand, as seen in obese women during pregnancy, alters fetal growth; however, the mechanism is unclear. To determine the role of adiponectin on placenta function and fetal growth, we used adiponectin knockout, adiponectin heterozygote that displays reduced adiponectin levels, and wild-type mice on a control diet or high fat/high sucrose (HF/HS) diet. Triglycerides (TGs) in the serum, liver, and placenta were measured using colorimetric assays. Gene expression was measured using quantitative RT-PCR. Adiponectin levels did not affect fetal weight, but it reduced adiponectin levels, increased fetal serum and placenta TG content. Wildtype dams on a HF/HS diet protected the fetuses from fatty acid overload as judged by increased liver TGs in dams and normal serum and liver TG levels in fetuses, while low adiponectin was associated with increased fetal liver TGs. Low maternal adiponectin increased the expression of genes involved in fatty acid transport; Lpl and Cd36 in the placenta. Adiponectin deficiency does not affect fetal growth but induces placental dysfunction and increases fetal TG load, which is enhanced with obesity. This could lead to imprinting effects on the fetus and the development of metabolic dysfunction in the offspring.

Ablation of uncoupling protein 3 affects interrelated factors leading to lipolysis and insulin resistance in visceral white adipose tissue.

The physiological role played by uncoupling protein 3 (UCP3) in white adipose tissue (WAT) has not been elucidated so far. In the present study, we evaluated the impact of the absence of the whole body UCP3 on WAT physiology in terms of ability to store triglycerides, oxidative capacity, response to insulin, inflammation, and adipokine production. Wild type (WT) and UCP3Knockout (KO) mice housed at thermoneutrality (30°C) have been used as the animal model. Visceral gonadic WAT (gWAT) from KO mice showed an impaired capacity to store triglycerides (TG) as indicated by its lowered weight, reduced adipocyte diameter, and higher glycerol release (index of lipolysis). The absence of UCP3 reduces the maximal oxidative capacity of gWAT, increases mitochondrial free radicals, and activates ER stress. These processes are associated with increased levels of monocyte chemoattractant protein-1 and TNF-α. The response of gWAT to in vivo insulin administration, revealed by (ser473)-AKT phosphorylation, was blunted in KO mice, with a putative role played by eif2a, JNK, and inflammation. Variations in adipokine levels in the absence of UCP3 were observed, including reduced adiponectin levels both in gWAT and serum. As a whole, these data indicate an important role of UCP3 in regulating the metabolic functionality of gWAT, with its absence leading to metabolic derangement. The obtained results help to clarify some aspects of the association between metabolic disorders and low UCP3levels.

An Avocado Extract Enriched in Mannoheptulose Prevents the Negative Effects of a High-Fat Diet in Mice.

Beginning at 16 weeks of age and continuing for 44 weeks, male C57BL/6J were fed either a control (CON) diet; a high-fat (HF) diet (60% unsaturated); or the HF diet containing an extract of unripe avocados (AvX) enriched in the 7-carbon sugar mannoheptulose (MH), designed to act as a glycolytic inhibitor (HF + MH). Compared to the CON diet, mice on the HF diet exhibited higher body weights; body fat; blood lipids; and leptin with reduced adiponectin levels, insulin sensitivity, VO2max, and falls from a rotarod. Mice on the HF + MH diet were completely protected against these changes in the absence of significant diet effects on food intake. Compared to the CON diet, oxidative stress was also increased by the HF diet indicated by higher levels of total reactive oxygen species, superoxide, and peroxynitrite measured in liver samples by electron paramagnetic resonance spectroscopy, whereas the HF + MH diet attenuated these changes. Compared to the CON, the HF diet increased signaling in the mechanistic target of the rapamycin (mTOR) pathway, and the addition of the MH-enriched AvX to this diet attenuated these changes. Beyond generating further interest in the health benefits of avocados, these results draw further new attention to the effects of this rare sugar, MH, as a botanical intervention for preventing obesity.

Preserved C‐peptide in survivors of COVID‐19: Post hoc analysis

Preserved <scp>C</scp>‐peptide in survivors of <scp>COVID</scp>‐19: Post hoc analysis

Адипонектин у больных с сахарным диабетом 2-го типа при нормальной массе тела

Установлено, что у больных сахарным диабетом 2-го типа на фоне нормальной массы тела средний уровень адипонектина (АН) в плазме крови, в отличие от больных с избыточной массой тела и ожирением, находится в пределах референтных норм. В то же время примерно у половины из них (54,5 %) уровень АН снижен. Подгруппа со сниженным уровнем АН отличается большим возрастом больных и длительностью диабета, а также повышением уровней триглицеридов и липопротеинов очень низкой плотности, более частым увеличением окружности талии. В то же время у больных сахарным диабетом 2-го типа с нормальной массой тела не выявлено достоверных ассоциативных связей между уровнем АН и показателями углеводного обмена — уровнем глюкозы в крови и инсулина натощак, индексом НОМА-IR.Полученные данные обосновывают необходимость своевременно выявлять и корригировать нарушения липидного обмена у больных сахарным диабетом 2-го типа с нормальной массой тела.

Adiponectin: a pleiotropic hormone with multifaceted roles.

Adipose tissue mostly composed of different types of fat is one of the largest endocrine organs in the body playing multiple intricate roles including but not limited to energy storage, metabolic homeostasis, generation of heat, participation in immune functions and secretion of a number of biologically active factors known as adipokines. The most abundant of them is adiponectin. This adipocite-derived hormone exerts pleiotropic actions and exhibits insulin-sensitizing, antidiabetic, anti-obesogenic, anti-inflammatory, antiatherogenic, cardio- and neuroprotective properties. Contrariwise to its protective effects against various pathological events in different cell types, adiponectin may have links to several systemic diseases and malignances. Reduction in adiponectin levels has an implication in COVID-19-associated respiratory failure, which is attributed mainly to a phenomenon called 'adiponectin paradox'. Ample evidence about multiple functions of adiponectin in the body was obtained from animal, mostly rodent studies. Our succinct review is entirely about multifaceted roles of adiponectin and mechanisms of its action in different physiological and pathological states.

Systematic review and meta-analysis of randomised, controlled trials on the effects of garlic supplementation on serum adiponectin and leptin levels.

Our aim in this meta-analysis was to determine the effect of garlic supplementation on adiponectin and leptin serum levels. A systematic search was conducted using PubMed, Scopus, ISI Web of Science and Cochrane Library for eligible trials up to November 2020. A fixed-effects model was used to pool calculated effect sizes. Five trials were included in the overall analysis. Our analysis showed that garlic supplementation did not significantly affect adiponectin (Hedges's: 0.20; 95% CI: -0.06, 0.47; P-values=.12) and leptin (Hedges's: 0.08; 95% CI: -0.26, 0.41; P-values=.65) concentrations in comparison with placebo. However, in the subgroup analysis, significantly increased serum adiponectin level was seen following garlic supplementation in trials with a mean age of participants ˂30years (Hedges's: 0.44; 95% CI: 0.01, 0.87; P-values=.04), the doses ˂1.5g/d (Hedges's: 0.38; 95% CI: 0.02, 0.71; P-values=.04) and trials with duration ≥8weeks (Hedges's: 0.48; 95% CI: 0.08, 0.89; P-values=.02). Overall, garlic supplementation could not change the circulatory adiponectin and leptin levels. Subgroup analyses showed a significant reduction in adiponectin levels in younger participants, longer duration and lower intervention dose. However, further studies are needed to confirm the present results.

Reduced adiponectin levels in patients with COVID-19 acute respiratory failure: A case-control study.

Hypoadiponectinemia is speculated to play a key role in the relationship between obesity and COVID‐19 respiratory failure. However, only one study has examined adiponectin levels in COVID‐19 patients, and none have investigated adiponectin levels strictly in patients with acute respiratory failure. In this study, we performed a retrospective case‐control study of adipokine levels in patients with acute respiratory failure caused by either COVID‐19 or other viral/bacterial source. All patients with COVID‐19 respiratory failure in the University of Virginia Biorepository and Tissue Research database were included. We also selected patients with non‐COVID‐19 infectious respiratory failure from the same biorepository to serve as a comparison cohort. Plasma adipokine levels were measured on three occasions during the first 72 hours of hospitalization. Twelve patients with COVID‐19 respiratory failure and 17 patients with other infectious respiratory failure were studied. Adiponectin levels were significantly lower in patients with COVID‐19 respiratory failure, even after adjustment for age, sex, BMI, and other covariates. In conclusion, adiponectin levels appear to be reduced in COVID‐19 respiratory failure. Larger studies are needed to confirm this report.