scholarly journals The influence of adiponectin on carbohydrates, lipids, and lipoproteins metabolism: analysis of signaling mechanisms

2021 ◽  
Vol 18 (2) ◽  
pp. 103-111
Author(s):  
D. A. Tanyanskiy ◽  
A. D. Denisenko
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
The Body ◽  
Molecular Forms ◽  
High Density Lipoproteins ◽  
Complex Nature ◽  
Satiety Hormone ◽  
Almost All ◽  
Lipids And Lipoproteins

Dysregulation of adipose tissue functions makes a significant contribution to the pathogenesis of metabolic syndrome, one of the most common diseases in recent years. Adipose tissue is an organ that secretes at least several dozen signaling molecules, adipokines. One of the most studied and at the same time mysterious adipokines is adiponectin. The latter is due to the lack of clear ideas about the biological role of this adipokine, the presence of its several molecular forms with different activity and several types of receptors to this adipokine localized in almost all cells of the body. The purpose of this review is to summarize and analyze the available information about the molecular mechanisms of the effect of adiponectin on metabolism of carbohydrates, lipids and lipoproteins. The literature search was conducted by the keywords "adiponectin" and "metabolic syndrome" in the Pubmed and Elibrary.ru databases for the period from 1995 to 2021.According to the results of the literature analysis, it is assumed that adiponectin is involved in energy metabolism as a «satiety» hormone that promotes the utilization and storage of energy-rich substrates, fatty acids and glucose, which prevents the development or mitigates the already developed insulin resistance. This reduces the amount of plasma triglycerides and increases the level of high-density lipoproteins in the plasma. Adiponectin affects metabolic processes by activating the AdipoR1-APPL1-LKB1-AMPK, AdipoR1-APPL1-p38, AdipoR2-PPARa cascades, and possibly by activating the ceramidase and phosphoinositide pathways and insulin signaling. In addition to the AdipoR1/2 receptors, the adhesion molecule T-cadherin may be involved in the transduction of the adiponectin signal in endothelial and muscle cells. The mechanisms of signal transduction from T-cadherin, as well as from AdipoR2, remain unclear. Studies on the mechanisms of the action of individual molecular forms of adiponectin are extremely rare. The analysis shows the complex nature of adiponectin signaling, many of the mechanisms of  which remain undiscovered, and it is possible that the near future will bring us significant progress in this area.

Kaempferol ameliorates symptoms of metabolic syndrome by improving blood lipid profile and glucose tolerance

2021 ◽  
Author(s):  
Ayasa Ochiai ◽  
Mahmoud Ben Othman ◽  
Kazuichi Sakamoto
Keyword(s):  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Molecular Mechanisms ◽  
Ldl Receptor ◽  
Blood Lipid ◽  
Apolipoprotein A1 ◽  
High Density Lipoproteins ◽  
Blood Lipid Profile ◽  
Beneficial Effects ◽  
Apoa1 Gene

Abstract Kaempferol (KPF) is a dietary polyphenol reported to have various beneficial effects on human health. However, its molecular mechanisms in regulating lipid and glucose metabolism are not fully understood. This study examined the effects of KPF on obesity, dyslipidemia, and diabetes in Tsumura, Suzuki, Obese Diabetes (TSOD) mice. The six-week administration of KPF decreased fat weight, serum total cholesterol, and low-density lipoproteins (LDLs); increased high-density lipoproteins (HDLs); and improved glucose tolerance. Additionally, KPF increased LDL receptor (LDLR) and apolipoprotein A1 (ApoA1) gene expression and decreased serum resistin levels. These findings suggest that the decrease in LDL and the increase in HDL caused by KPF may be due to increases in hepatic LDLR and ApoA1 expression, respectively. Furthermore, it is possible that the improvement in glucose tolerance by KPF may occur via resistin reduction. These mechanisms may be parts of complex mechanism by which KPF improves metabolic syndrome.

Abstract 1125: Mulberry Leaf Ameliorates The Production Of Adipocytokines By Inhibiting Oxidative Stress In White Adipose Tissue In db/db Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Masayuki Sugimoto ◽  
Hidenori Arai ◽  
Yukinori Tamura ◽  
Toshinori Murayama ◽  
Koh Ono ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Metabolic Disorders ◽  
The Body ◽  
Mulberry Leaf ◽  
The Metabolic Syndrome ◽  
Pparγ Agonist ◽  
Tnf Α

Mulberry leaf (ML) is commonly used to feed silkworms. Previous study showed that ML ameliorates atherosclerosis. However, its mechanism is not completely understood. Because dysregulated production of adipocytokines is involved in the development of the metabolic syndrome and cardiovascular disease, we examined the effect of ML on the production of adipocytokines and metabolic disorders related to the metabolic syndrome, and compared its effect with that of a PPARγ agonist, pioglitazone (Pio). By treating obese diabetic db/db mice with ML, Pio, and their combination, we investigated the mechanism by which they improve metabolic disorders. In this study, db/+m (lean control) and db/db mice were fed a standard diet with or without 3% (w/w) ML and/or 0.01% (w/w) Pio for 12 weeks from 9 weeks of age. At the end of the experiment we found that ML decreased plasma glucose and triglyceride by 32% and 30%, respectively. Interestingly, administration of ML in addition to Pio showed additive effects; further 40% and 30% reduction in glucose and triglyceride compared with Pio treatment, respectively. Moreover, administration of ML in addition to Pio suppressed the body weight increase by Pio treatment and reduced visceral/subcutaneous fat ratio by 20% compared with control db/db mice. Importantly, ML treatment increased expression of adiponectin in white adipose tissue (WAT) by 40%, which was only found in db/db mice, not in control db/+m mice. Combination of ML and Pio increased plasma adiponectin concentrations by 25% and its expression in WAT by 17% compared with Pio alone. In contrast, ML decreased expression of TNF-α and MCP-1 by 25% and 20%, respectively, and the addition of Pio resulted in a further decrease of these cytokines by about 45%. To study the mechanism, we examined the role of oxidative stress. ML decreased the amount of lipid peroxides by 43% and the expression of NADPH oxidase subunits in WAT, which was consistent with the results of TNF-α and MCP-1. Thus our results indicate that ML ameliorates adipocytokine dysregulation by inhibiting oxidative stress in WAT of obese mice, and that ML may have a potential for the treatment of the metabolic syndrome as well as reducing adverse effects of Pio.

scholarly journals Exercise Induced Adipokine Changes and the Metabolic Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
Saeid Golbidi ◽  
Ismail Laher
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
The Body ◽  
Beneficial Effects ◽  
The Metabolic Syndrome ◽  
Before And After ◽  
Inflammatory State ◽  
Exercise Induced

The lack of adequate physical activity and obesity created a worldwide pandemic. Obesity is characterized by the deposition of adipose tissue in various parts of the body; it is now evident that adipose tissue also acts as an endocrine organ capable of secreting many cytokines that are though to be involved in the pathophysiology of obesity, insulin resistance, and metabolic syndrome. Adipokines, or adipose tissue-derived proteins, play a pivotal role in this scenario. Increased secretion of proinflammatory adipokines leads to a chronic inflammatory state that is accompanied by insulin resistance and glucose intolerance. Lifestyle change in terms of increased physical activity and exercise is the best nonpharmacological treatment for obesity since these can reduce insulin resistance, counteract the inflammatory state, and improve the lipid profile. There is growing evidence that exercise exerts its beneficial effects partly through alterations in the adipokine profile; that is, exercise increases secretion of anti-inflammatory adipokines and reduces proinflammatory cytokines. In this paper we briefly describe the pathophysiologic role of four important adipokines (adiponectin, leptin, TNF-α, and IL-6) in the metabolic syndrome and review some of the clinical trials that monitored these adipokines as a clinical outcome before and after exercise.

scholarly journals Pathophysiological justification of age- and gender-dependent morphological changes in the adipose tissue in rat models of metabolic syndrome

2021 ◽  
Author(s):  
Natalia A. Shutova ◽  
Olha V. Nikolaieva ◽  
Irina Yu. Kuzmina ◽  
Olena O. Pavlova ◽  
Inna O. Sulhdost
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Chronic Inflammation ◽  
Morphological Changes ◽  
Regional Distribution ◽  
Morphological Characteristics ◽  
The Body ◽  
Age And Gender ◽  
White Rats ◽  
And Gender

Introduction: The mechanisms of metabolic syndrome (MS) is one of the urgent issues in medicine. Regional distribution of the adipose tissue should be diagnosed at clinical examination, as the morphometric parameters of the cells of the active adipose tissue components may indicate the metabolic state. Aim: The aim of the study was to evaluate the differences in morphological and histological parameters of the adipose tissue associated with the development of MS in animals of different ages and gender. Material and methods: An experimental study was carried out on 144 WAG/G Sto white rats, divided into three study groups. Group 1 included young immature rats, 3 months old; group 2 consisted of 48 sexually mature rats, aged 5–6 months; group 3 consisted of 48 old rats, 18 months old. Each group was divided into 2 subgroups, control and experimental, and was additionally divided according to gender. Results and discussion: The body mass indices and specific weights of mesenteric, epididymal, retroperitoneal and subcutaneous adipose tissue were determined in rats, as well as morphological characteristics of adipocytes of the adipose tissue. It was shown that histological and morphological changes in the adipose tissue of the animals were age- and gender-dependent, and that obesity is associated with chronic inflammation of the adipose tissue. Conclusions: The results of the study can be used for further determination of possible age and gender differences in the adipose tissue involvement in the development of chronic inflammation, as well as monitoring and correction of adipose tissue dysfunction in MS.

scholarly journals Lymphatic system and adipose tissue: Crosstalk in health and disease

2021 ◽  
Vol 18 (3) ◽  
pp. 336-344
Author(s):  
V. V. Klimontov ◽  
D. M. Bulumbaeva
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Inflammatory Cells ◽  
The Body ◽  
Push Button ◽  
Secondary Lymphedema

The lymphatic system (LS) is one of the main integrative systems of the body, providing protective and transport functions. In recent years, interactions between LS and adipose tissue (AT) have been of particular interest. Lymphatic vessels play an important role in metabolic and regulatory functions of AT, acting as a collector of lipolysis products and adipokines. In its turn, hormones and adipocytokines that produced in adipocytes (including leptin, adiponectin, IL-6, TNF-α, etc.) affect the function of lymphatic endothelial cells and control the growth of lymphatic vessels. Cooperation between LS and AT becomes pathogenetically and clinically important in lymphedema and obesity. It is known that both primary and secondary lymphedema are characterized by increased fat accumulation which is associated with the severity of lymphostasis and inflammation. Similarly, in obesity, the drainage function of LS is impaired, which is accompanied by perilymphatic mononuclear infiltration in the AT. The development of these changes is facilitated by endocrine dysfunction of adipocytes and impaired production of adipocytokines. The increase in the production of inflammatory mediators and the disruption of the traffic of inflammatory cells causes a further deterioration in the outflow of interstitial fluid and exacerbates the inflammation of the AT, thereby forming a vicious circle. The role of lymphangiogenesis in AT remodeling in obesity needs further research. Another promising area of research is the study of the role of intestinal LS in the development of obesity and related disorders. It has been shown that the transport of chylomicrons from the intestine depends on the expression of a number of molecular mediators (VEGF-C, DLL-4, neuropilin-1, VEGFR-1, CD36/FAT, etc.)in the endotheliocytes of the intestinal lymphatic vessels, as well as the functioning of «push-button» and “zippering” junctions between endothelial cells. New approach to the treatment of obesity based on blockade of lymphatic chylomicrontransport has been experimentally substantiated. Further identification of the molecular mechanisms and signaling pathways that determine the remodeling of AT in lymphedema and obesity are likely to provide new approaches to the treatment of these diseases.

Features of metabolic and hormonal abnormalities in women with metabolic syndrome at the stage pregrada

2017 ◽  
pp. 57-61
Author(s):  
O.A. Dyndar ◽  
Keyword(s):  
Metabolic Syndrome ◽  
Body Mass Index ◽  
Body Mass ◽  
Reproductive System ◽  
The Body ◽  
Reproductive Age ◽  
High Density Lipoproteins ◽  
Women Of Reproductive Age ◽  
Female Population ◽  
Number Of Components

The problem of obesity and metabolic syndrome among the female population of Ukraine is extremely important, given the current trend toward increasing age of realization of reproductive function,. The prevalence of metabolic syndrome among women of reproductive age is 6–35%, fertility problems are found in 30-35% of women. The objective: to study the characteristics of metabolic disorders and hormonal condition of the reproductive system in women with obesity and the metabolic syndrome on pregravidarity stage depending on the body mass index and severity of metabolic syndrome. Patients and methods. We examined a total of 124 women with obesity and metabolic syndrome that appealed on pregravidar stage and 53 women who had no history of somatic and gynecological pathology. Antropometric studies, determination of blood pressure, examination of carbohydrate and lipid metabolism, evaluation of the endocrine status of the reproductive system, ultrasound examination of small pelvis organs were done. Results. In women of reproductive age, we observed increase of total cholesterol, triglycerides, low-density lipoproteins and decrease high-density lipoproteins, with a predominance of IIb and IV types of dyslipidemia. Insulin resistance was diagnosed in 28.3% of women And 47.4% – II and in 69.7% with III degree of obesity. Metabolic syndrome was diagnosed in 79.2% of patients with obesity of I, in 94.7% – II 100% III. The number of components of metabolic syndrome correlate directly proportional to the severity of obesity. The index of fertility with III degree of obesity increased to 2.7, hypoestrogenia marked with And hyperestrogenia from 50.7% of women in II and III degree of obesity, progesterona failure identified at 66.9%, hyperandrogenism in 58.8%, reduced sex-binding globulin in 83.0% of the observations. Conclusion. Pathological changes of the hormonal status of the female reproductive system on prepregnansy stage is directly proportional to depend on the body mass index number of components of metabolic syndrome and dysmetabolic disorders. Key words: obesity, metabolic syndrome, pregnancy planning.

scholarly journals Lipid-Induced Mechanisms of Metabolic Syndrome

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Yulia K. Denisenko ◽  
Oxana Yu Kytikova ◽  
Tatyana P. Novgorodtseva ◽  
Marina V. Antonyuk ◽  
Tatyana A. Gvozdenko ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Inflammatory Process ◽  
Molecular Mechanisms ◽  
Insulin Response ◽  
The Body ◽  
Diagnostic Methods ◽  
The Other ◽  
Prevention And Treatment ◽  
The One

Metabolic syndrome (MetS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnosis, approaches to the prevention, and treatment of this pathology. Insulin resistance (IR) is the crucial cause of the MetS pathogenesis, which develops against the background of abdominal obesity. In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. On the one hand, the lack of n-3 polyunsaturated fatty acids (PUFAs) in the body leads to impaired molecular mechanisms of glucose transport, the formation of unresolved inflammation. On the other hand, excessive formation of free fatty acids (FFAs) underlies the development of oxidative stress and mitochondrial dysfunction in MetS. Understanding the molecular mechanisms of the participation of FAs and their metabolites in the pathogenesis of MetS will contribute to the development of new diagnostic methods and targeted therapy for this disease. The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS.

scholarly journals Tofogliflozin Improves Insulin Resistance in Skeletal Muscle and Accelerates Lipolysis in Adipose Tissue in Male Mice

Endocrinology ◽  
2015 ◽  
Vol 157 (3) ◽  
pp. 1029-1042 ◽  
Author(s):  
Atsushi Obata ◽  
Naoto Kubota ◽  
Tetsuya Kubota ◽  
Masahiko Iwamoto ◽  
Hiroyuki Sato ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
The Body ◽  
High Fat ◽  
Ad Libitum

Abstract Sodium glucose cotransporter 2 inhibitors have attracted attention as they exert antidiabetic and antiobesity effects. In this study, we investigated the effects of tofogliflozin on glucose homeostasis and its metabolic consequences and clarified the underlying molecular mechanisms. C57BL/6 mice were fed normal chow containing tofogliflozin (0.005%) for 20 weeks or a high-fat diet containing tofogliflozin (0.005%) for 8 weeks ad libitum. In addition, the animals were pair-fed in relation to controls to exclude the influence of increased food intake. Tofogliflozin reduced the body weight gain, mainly because of fat mass reduction associated with a diminished adipocyte size. Glucose tolerance and insulin sensitivity were ameliorated. The serum levels of nonesterified fatty acid and ketone bodies were increased and the respiratory quotient was decreased in the tofogliflozin-treated mice, suggesting the acceleration of lipolysis in the white adipose tissue and hepatic β-oxidation. In fact, the phosphorylation of hormone-sensitive lipase and the adipose triglyceride lipase protein levels in the white adipose tissue as well as the gene expressions related to β-oxidation, such as Cpt1α in the liver, were significantly increased. The hepatic triglyceride contents and the expression levels of lipogenic genes were decreased. Pair-fed mice exhibited almost the same results as mice fed an high-fat diet ad libitum. Moreover, a hyperinsulinemic-euglycemic clamp revealed that tofogliflozin improved insulin resistance by increasing glucose uptake, especially in the skeletal muscle, in pair-fed mice. Taken together, these results suggest tofogliflozin ameliorates insulin resistance and obesity by increasing glucose uptake in skeletal muscle and lipolysis in adipose tissue.

scholarly journals Features and relationships of metabolic syndrome components in men with androgen deficiency. Part 2. Disorders of carbohydrate and purine metabolism. Retrospective study data

2020 ◽  
Author(s):  
Z. Sh. Pavlova ◽  
V. Yu. Grevina
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Body Composition ◽  
Adipose Tissue ◽  
Negative Correlation ◽  
Testosterone Level ◽  
Purine Metabolism ◽  
The Body ◽  
Total Testosterone ◽  
Androgen Deficiency

Introduction. There are few epidemiological data on violations of purine and carbohydrate metabolism in association with testosterone deficiency in men with overweight due to adipose tissue and metabolic syndrome (MS).Aim: to study the relationships between disturbances in carbohydrate and purine metabolism and testosterone level in men with excess adipose tissue and MS.Materials and Мethods. There were enrolled 64 overweight men to the study. The patients were divided into 3 groups based on the body mass index (BMI): group 1 – with overweight (n = 24), group 2 – with the first degree of obesity (n = 21), group 3 – with the second and third degree of obesity (n = 19). A correlation analysis was carried out between the data of carbohydrate and purine metabolism in relation to testosterone level and body composition, as well as additionally assessing the level of inter-group difference.Results. The relationship between the parameters of carbohydrate and purine metabolism and the level of total testosterone has been identified, and it's formed against the background of overdeveloped adipose tissue. A weak negative correlation was found across the sample between testosterone and glucose, insulin, and the НОМА-IR (Homeostasis Model Assessment of Insulin Resistance) index. That is, the higher the level of glucose, the НОМА-IR index, the lower the testosterone level. In addition, it was noted that an increase in BMI caused higher insulin levels. The number of patients with fasting blood glucose levels above 5.6 mmol/L and insulin resistance also increased. In the group with I degree of obesity, a negative correlation was found between the levels of total testosterone and uric acid.Conclusion. Thus, the thesis is confirmed that the more significant the violation of carbohydrate and purine metabolism, the more significant androgenic deficiency. It is obvious that the most effective solution in choosing a strategy for treating androgen deficiency and disorders of carbohydrate and purine metabolism in overweight men is to normalize body composition and get rid of excess adipose tissue.

scholarly journals Role of dysfunctional adipocytes in cholesterol-induced nonobese metabolic syndrome

2018 ◽  
Vol 60 (4) ◽  
pp. 309-323 ◽  
Author(s):  
Jiung-Pang Huang ◽  
Sheng-Chieh Hsu ◽  
Yaa-Jyuhn James Meir ◽  
Po-Shiuan Hsieh ◽  
Chih-Chun Chang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Macrophage Polarization ◽  
The Body ◽  
Hormone Sensitive Lipase ◽  
Whole Body ◽  
Sprague Dawley ◽  
Nonesterified Fatty Acids ◽  
Raw264.7 Macrophages ◽  
Antioxidant Defense Systems

Many studies have reported the causes of obese metabolic syndrome (MS); however, the causes of nonobese MS (NMS) remain unknown. In this study, we demonstrated that inflamed dysfunctional adipose tissue plays a crucial role in cholesterol-induced NMS. Control (C), high cholesterol (HC) and HC with 10% fructose in drinking water (HCF) diets were fed to Sprague–Dawley rats for 12 weeks. After 12 weeks, the body weights of the C- and HC-fed rats were comparable, but the weights of the HCF-fed rats were relatively low. Cholesterol caused metabolic problems such as high blood pressure, hypercholesterolemia and hypoinsulinemia. The HCF-fed rats exhibited whole-body insulin resistance with low circulating high-density lipoprotein levels. Increases in the tumor necrosis factor α level in the plasma, the number of CD68+ macrophages and the free nuclear factor-κB level in gonadal white adipose tissue (gWAT) resulted in local inflammation, which appeared as inflamed dysfunctional gWAT. Reduced superoxide dismutases (SODs) deteriorate natural antioxidant defense systems and induce reactive oxygen species in gWAT. Dysregulation of plasma levels of catecholamine, adipokines (leptin and adiponectin), hormone-sensitive lipase and perilipin in cholesterol-induced inflamed adipose tissue contributed to increased lipolysis and increased circulating nonesterified fatty acids. Cholesterol activated inflammation, lipolysis and cell death in 3T3-L1 adipocytes. Moreover, Chol-3T3-CM reduced the population of M2-type Raw264.7 macrophages, indicating that the macrophage polarization is mediated by cholesterol. Together, our findings indicate that inflamed dysfunctional adipocytes are critical in NMS, supporting the development of anti-inflammatory agents as potential therapeutic drugs for treating NMS.

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