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1.
Hum Genet ; 139(4): 447-459, 2020 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-32076828

RESUMEN

Low-density lipoprotein receptor-related protein 6 (LRP6) is a member of the low-density lipoprotein receptors (LDLRs) family and accumulating evidence points to the critical role of LRP6 in cardiovascular health and homeostasis. In addition to presenting the well-appreciated roles in canonical signaling regulating blood pressure, blood glucose, lipid metabolism, atherosclerosis, cardiac valve disease, cardiac development, Alzheimer's disease and tumorigenesis, LRP6 also inhibits non-canonical Wnt signals that promote arterial smooth muscle cell proliferation and vascular calcification. Noticeably, the role of LRP6 is displayed in cardiometabolic disease, an increasingly important clinical burden with aging and obesity. The prospect for cardiovascular diseases treatment via targeting LRP6-mediated signaling pathways may improve central blood pressure and lipid metabolism, and reduce neointima formation and myocardial ischemia-reperfusion injury. Thus, a deep and comprehensive understanding of LRP6 structure, function and signaling pathways will contribute to clinical diagnosis, therapy and new drug development for LRP6-related cardiovascular diseases.


Asunto(s)
Enfermedades Cardiovasculares , Proteína-6 Relacionada a Receptor de Lipoproteína de Baja Densidad , Transducción de Señal , Calcificación Vascular , Vía de Señalización Wnt , Envejecimiento/metabolismo , Envejecimiento/patología , Animales , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/patología , Enfermedades Cardiovasculares/terapia , Humanos , Proteína-6 Relacionada a Receptor de Lipoproteína de Baja Densidad/química , Proteína-6 Relacionada a Receptor de Lipoproteína de Baja Densidad/metabolismo , Músculo Liso Vascular/metabolismo , Músculo Liso Vascular/patología , Miocitos del Músculo Liso/metabolismo , Miocitos del Músculo Liso/patología , Obesidad/metabolismo , Obesidad/patología , Relación Estructura-Actividad , Calcificación Vascular/diagnóstico , Calcificación Vascular/metabolismo , Calcificación Vascular/patología , Calcificación Vascular/terapia
2.
Adv Clin Exp Med ; 29(1): 79-84, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-32017476

RESUMEN

BACKGROUND: Visfatin is one of the pro-inflammatory adipokines secreted by adipose tissue cells. Recent scientific research has drawn attention to the role of adipokines in the pathophysiology of metabolic disorders and their association with inflammatory diseases, including psoriasis. Visfatin may be one of the important links explaining the connection between psoriasis and diseases which are components of metabolic syndrome. OBJECTIVES: The aim of this study was to assess the serum visfatin concentration in patients with psoriasis and to evaluate its possible correlations with parameters of metabolic syndrome and the clinical severity of psoriasis. MATERIAL AND METHODS: A group of 102 patients with psoriasis and a control group of 40 healthy subjects were examined. The clinical severity of psoriasis was assessed according to Psoriasis Area and Severity Index), BSA (Body Surface Area) and DLQI (Dermatology Life Quality Index) indicators, the presence and type of obesity, and hypertension. In both the study and control groups, laboratory tests (C-reactive protein (CRP), glucose concentration, total cholesterol, low-density-lipoprotein (LDL0 cholesterol, high-density-lipoprotein (HDL) cholesterol, and triglycerides (TG)) were performed and serum visfatin concentrations were determined. The clinical data, results of laboratory tests and visfatin concentrations were then subjected to statistical analysis. RESULTS: There was a significantly higher concentration of visfatin in the psoriatic patients (p < 0.001) than in the control group. Significant positive correlations between visfatin concentration and PASI (p = 0.008) and BSA (p = 0.007) were observed. In the psoriatic group, there were positive correlations between the concentrations of visfatin and the concentrations of CRP (p = 0.008) and total cholesterol (p = 0.002). Visfatin concentration was elevated in the psoriatic patients who had elevated total cholesterol (p = 0.001), LDL cholesterol (p = 0.012) and TG levels (p = 0.001) compared to the psoriatic patients with normal levels of these lipid profile components. CONCLUSIONS: The results indicate the possible participation of visfatin in pathophysiological and inflammatory processes in the course of psoriasis. Adipokines may be an important link connecting psoriasis with coexisting metabolic disorders.


Asunto(s)
Síndrome Metabólico , Nicotinamida Fosforribosiltransferasa , Psoriasis , Estudios de Casos y Controles , HDL-Colesterol , Humanos , Masculino , Síndrome Metabólico/metabolismo , Nicotinamida Fosforribosiltransferasa/sangre , Obesidad/metabolismo , Psoriasis/metabolismo
3.
J Agric Food Chem ; 68(4): 1007-1014, 2020 Jan 29.
Artículo en Inglés | MEDLINE | ID: mdl-31914311

RESUMEN

Induction of beige adipocytes in white adipose tissue (WAT) is a potential therapeutic target for the treatment of obesity because beige adipocytes release excess energy via uncoupling-protein-1-associated thermogenesis. In this study, we investigated how artepillin C (ArtC) promotes thermogenesis in vivo. We demonstrated that 28 day administration of ArtC (10 mg/kg of body weight) to mice significantly induced thermogenesis in beige adipocytes in inguinal WAT (iWAT) and suppressed reductions in core body temperature induced by cold exposure at 4 °C. Moreover, ArtC-induced thermogenesis in iWAT was significantly inhibited by treatment with a creatine metabolism inhibitor, and ArtC significantly upregulated the expression of creatine-metabolism-related enzymes in the thermogenic pathway. These results indicate that ArtC induces thermogenesis in beige adipocytes in iWAT, and the observed ArtC-induced thermogenesis is associated with the creatine-metabolism-related thermogenic pathway, which is characteristically observed in beige adipocytes.


Asunto(s)
Tejido Adiposo Blanco/efectos de los fármacos , Creatina/metabolismo , Obesidad/tratamiento farmacológico , Fenilpropionatos/administración & dosificación , Própolis/análisis , Termogénesis/efectos de los fármacos , Adipocitos Beige/efectos de los fármacos , Adipocitos Beige/metabolismo , Tejido Adiposo Blanco/metabolismo , Animales , Temperatura Corporal , Brasil , Humanos , Masculino , Ratones , Ratones Endogámicos C57BL , Obesidad/metabolismo , Obesidad/fisiopatología , Própolis/administración & dosificación
4.
Adv Clin Chem ; 94: 155-218, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31952571

RESUMEN

Bone and skeletal muscle are integrated organs and their coupling has been considered mainly a mechanical one in which bone serves as attachment site to muscle while muscle applies load to bone and regulates bone metabolism. However, skeletal muscle can affect bone homeostasis also in a non-mechanical fashion, i.e., through its endocrine activity. Being recognized as an endocrine organ itself, skeletal muscle secretes a panel of cytokines and proteins named myokines, synthesized and secreted by myocytes in response to muscle contraction. Myokines exert an autocrine function in regulating muscle metabolism as well as a paracrine/endocrine regulatory function on distant organs and tissues, such as bone, adipose tissue, brain and liver. Physical activity is the primary physiological stimulus for bone anabolism (and/or catabolism) through the production and secretion of myokines, such as IL-6, irisin, IGF-1, FGF2, beside the direct effect of loading. Importantly, exercise-induced myokine can exert an anti-inflammatory action that is able to counteract not only acute inflammation due to an infection, but also a condition of chronic low-grade inflammation raised as consequence of physical inactivity, aging or metabolic disorders (i.e., obesity, type 2 diabetes mellitus). In this review article, we will discuss the effects that some of the most studied exercise-induced myokines exert on bone formation and bone resorption, as well as a brief overview of the anti-inflammatory effects of myokines during the onset pathological conditions characterized by the development a systemic low-grade inflammation, such as sarcopenia, obesity and aging.


Asunto(s)
Huesos/metabolismo , Citocinas/metabolismo , Músculo Esquelético/metabolismo , Envejecimiento/metabolismo , Animales , Ejercicio , Homeostasis , Humanos , Inflamación/metabolismo , Obesidad/metabolismo
5.
Adv Clin Chem ; 94: 261-321, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31952573

RESUMEN

Studies have linked obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD) and dementia. Their relationship to the incidence and progression of these disease states suggests an interconnected pathogenesis involving chronic low-grade inflammation and oxidative stress. Metabolic syndrome represents comorbidities of central obesity, insulin resistance, dyslipidemia, hypertension and hyperglycemia associated with increased risk of type 2 diabetes, NAFLD, atherosclerotic CVD and neurodegenerative disease. As the socioeconomic burden for these diseases has grown signficantly with an increasing elderly population, new and alternative pharmacologic solutions for these cardiometabolic diseases are required. Adipose tissue, skeletal muscle and liver are central endocrine organs that regulate inflammation, energy and metabolic homeostasis, and the neuroendocrine axis through synthesis and secretion of adipokines, myokines, and hepatokines, respectively. These organokines affect each other and communicate through various endocrine, paracrine and autocrine pathways. The ultimate goal of this review is to provide a comprehensive understanding of organ crosstalk. This will include the roles of novel organokines in normal physiologic regulation and their pathophysiological effect in obesity, metabolic syndrome, type 2 diabetes, CVD, NAFLD and neurodegenerative disorders.


Asunto(s)
Adipoquinas/metabolismo , Enfermedades Cardiovasculares/metabolismo , Diabetes Mellitus Tipo 2/metabolismo , Síndrome Metabólico/metabolismo , Enfermedades Neurodegenerativas/metabolismo , Obesidad/metabolismo , Humanos
6.
J Agric Food Chem ; 68(3): 779-787, 2020 Jan 22.
Artículo en Inglés | MEDLINE | ID: mdl-31894986

RESUMEN

The chain length of fructan determines its different physiological effects. This study is to explore the effects of low-performance inulin [LPI, degree of polymerization (DP) ≤ 9] and high-performance inulin (HPI, DP ≥ 23) on obesity-associated liver injury of high-fat diet (HFD) feeding mice and its underlying mechanism. Eight weeks of supplementation of C57BL/6J mice with HPI, relative to LPI (p < 0.05), caused the more efficient improvement against the HFD-induced liver insulin resistance through activating IRS1/PI3K/Akt pathway and reduced protein expressions of inflammatory factors nuclear factor-kappaB (NF-κB) and interleukin-6 (IL-6) in the liver. HPI exhibited the more positive effects on liver steatosis by inhibiting acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and sterol regulatory element binding protein 1 (SREBP1) in comparison with LPI (p < 0.05). HPI also increased acetic acid, propionic acid, and butyric acid levels in the colon of HFD-fed mice (p < 0.05). Compared to LPI, HPI feeding of HFD-fed mice led to the more effective decrease in the Firmicutes abundance from 72.1% to 34.5%, but a more significant increase in the Bacteroidetes population from 19.8 to 57.1% at the phyla level, and increased the abundance of Barnesiella, Bacteroides, and Parabacteroides at the genus level (p < 0.05). Depending on DP, HPI exerts the more positive regulation on liver injury and gut microbiota dysfunction than LPI.


Asunto(s)
Disbiosis/tratamiento farmacológico , Microbioma Gastrointestinal/efectos de los fármacos , Inulina/administración & dosificación , Inulina/química , Hígado/lesiones , Obesidad/tratamiento farmacológico , Animales , Bacterias/clasificación , Bacterias/efectos de los fármacos , Bacterias/genética , Bacterias/aislamiento & purificación , Dieta Alta en Grasa/efectos adversos , Suplementos Dietéticos/análisis , Disbiosis/genética , Disbiosis/metabolismo , Disbiosis/microbiología , Humanos , Interleucina-6/genética , Interleucina-6/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Obesos , FN-kappa B/genética , FN-kappa B/metabolismo , Obesidad/genética , Obesidad/metabolismo , Obesidad/microbiología , Fosfatidilinositol 3-Quinasas/genética , Fosfatidilinositol 3-Quinasas/metabolismo , Polimerizacion
7.
J Agric Food Chem ; 68(7): 2256-2262, 2020 Feb 19.
Artículo en Inglés | MEDLINE | ID: mdl-31927923

RESUMEN

Fat deposition is one of the most important economic traits of pigs. Decreasing the subcutaneous fat and increasing the intramuscular fat are believed to be an effective way to improve pork quality, which is one of the main goals of pig breeding. Identifying key genes that control porcine lipid metabolism is essential for achieving this goal. Apolipoprotein R (apoR) was identified as the crucial molecule in the process of pig adipose reduction by clenbuterol. In this study, transgenic mice with adipose-tissue-specific overexpression of pig apoR (apoR mice) were constructed. The apoR mice gained less weight than wild-type (WT) mice after 18 weeks of feeding a high-fat diet. A comparison of organs between the two genotypes revealed that the weight of white adipose tissue, including inguinal and epididymal fat tissue, was significantly decreased and the weight of liver tissue was increased in apoR mice compared with WT mice. Glucose and insulin intolerance tests showed that the glucose metabolism of apoR mice was similar to that of WT mice. Histological staining proved that the adipocytes of apoR mice had a reduced average size, and gene expression analysis indicated that lipolysis in the adipose tissue of apoR mice was enhanced. Finally, the primary culture of inguinal adipocytes revealed that apoR promotes lipolysis via the Erk1/2 pathway. Taken together, the results indicate that adipose-tissue-specific expression of pig apoR protects mice from diet-induced obesity by enhancing lipolysis.


Asunto(s)
Tejido Adiposo/metabolismo , Apolipoproteínas/genética , Obesidad/genética , Obesidad/prevención & control , Adipocitos/metabolismo , Animales , Apolipoproteínas/metabolismo , Dieta Alta en Grasa/efectos adversos , Quinasas MAP Reguladas por Señal Extracelular/genética , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Glucosa/metabolismo , Lipólisis , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Obesidad/metabolismo , Obesidad/fisiopatología , Porcinos
8.
J Agric Food Chem ; 68(7): 2183-2192, 2020 Feb 19.
Artículo en Inglés | MEDLINE | ID: mdl-31984741

RESUMEN

Obesity is a global chronic disease linked to various diseases. Increased consumption of added sugars, especially in beverages, is a key contributor to the obesity epidemic. It is essential to reduce or replace sugar intake with low-calorie sweeteners. Here, a natural sweet protein, 3M-brazzein, was investigated as a possible sugar substitute. Mice were exposed to 3M-brazzein or 10% sucrose of equivalent sweetness, in drinking water to mimic human obesity development over 15 weeks. Consumption of 3M-brazzein in liquid form did not cause adiposity hypertrophy, resulting in 33.1 ± 0.4 g body weight and 0.90 ± 0.2 mm fat accumulation, which were 35.9 ± 0.7 g (p = 0.0094) and 1.53 ± 0.067 mm (p = 0.0031), respectively, for sucrose supplement. Additionally, 3M-brazzein did not disrupt glucose homeostasis or affect insulin resistance and inflammation. Due to its naturally low-calorie content, 3M-brazzein could also be a potential sugar substitute that reduces adiposity.


Asunto(s)
Enfermedades Metabólicas/metabolismo , Obesidad/metabolismo , Proteínas de Plantas/metabolismo , Edulcorantes/metabolismo , Adiposidad , Animales , Peso Corporal , Ingestión de Energía , Humanos , Resistencia a la Insulina , Kluyveromyces/genética , Kluyveromyces/metabolismo , Masculino , Enfermedades Metabólicas/inmunología , Enfermedades Metabólicas/fisiopatología , Ratones , Ratones Endogámicos C57BL , Obesidad/inmunología , Obesidad/fisiopatología , Proteínas de Plantas/genética
9.
Gene ; 733: 144353, 2020 Apr 05.
Artículo en Inglés | MEDLINE | ID: mdl-31978509

RESUMEN

OBJECTIVE: The present study investigates the association of dietary intake of fruit and green Vegetables with PTEN and P53 mRNA gene expression in visceral (VAT) and subcutaneous adipose tissues (SAT) of obese and non-obese adults. METHODS: VAT and SAT were obtained from 151 individuals, aged ~40 years, who had undergone elective abdominal surgery. The participants were grouped according to their body mass index (BMI), as obese (BMI > 30 kg/m2) and non-obese (BMI = 18.5-30 kg/m2). Dietary intakes were obtained using a valid and reliable food-frequency questionnaire (FFQ). Real-time PCR was carried out for PTEN and P53 mRNA expressions. Associations between expression levels and dietary parameters were analyzed. RESULTS: P53 mRNA expression of obese participants was significantly higher than the non-obese, only in VAT (p < 0.001). After adjusting for total energy intake, age and BMI, fruit intake was inversely associated with P53 gene expression in both VAT (ß = -0.38, P = 0.01) and SAT (ß = -0.35, P = 0.03) among non-obese participants. Furthermore, fruit consumption was inversely associated with P53 gene expression in obese individuals, only in VAT (ß = -0.21, P = 0.05). More so, intake of green vegetables in obese subjects was negatively associated with P53 gene expression in VAT (ß = -0.27, P = 0.01) and SAT (ß = -0.28, P < 0.001). On the other hand, after adjustment for total energy intake, age and BMI, a positive association was observed between fruit intake and PTEN in VAT (ß = 0.27, P = 0.01) and SAT (ß = 0.34, P < 0.001) among obese participants. In addition, dietary consumption of fruits in non-obese individuals was negatively associated withPTEN expression in SAT (ß = -0.48, P < 0.001). CONCLUSION: Dietary intake of fruit and green vegetables was associated with P53 gene expression in VAT and SAT of obese participants, suggesting their protective role in regulating P53 mRNA expression in adipose tissue. Furthermore, higher fruit intake was inversely associated with PTEN mRNA levels in non-obese participants, implying the anti-adipogenic role of PTEN gene expression.


Asunto(s)
Tejido Adiposo/metabolismo , Frutas , Grasa Intraabdominal/metabolismo , Obesidad/metabolismo , Fosfohidrolasa PTEN/metabolismo , Grasa Subcutánea/metabolismo , Proteína p53 Supresora de Tumor/metabolismo , Verduras , Adulto , Estudios de Casos y Controles , Estudios Transversales , Femenino , Regulación de la Expresión Génica , Humanos , Masculino , Persona de Mediana Edad , Obesidad/dietoterapia , Obesidad/genética , Obesidad/patología , Fosfohidrolasa PTEN/genética , ARN Mensajero/genética , ARN Mensajero/metabolismo , Proteína p53 Supresora de Tumor/genética
10.
J Sci Food Agric ; 100(3): 897-903, 2020 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-31588996

RESUMEN

Tea polyphenols (TP) are the main components in tea. Studies in vitro have shown they have significant biological activity; however, the results are inconsistent with experiments in vivo. For the low bioavailability, most TP are thought to remain in the gut and metabolized by intestinal bacteria. In the gut, the unabsorbed TP are metabolized to a variety of derivative products by intestinal flora, which may accumulate to exert beneficial effects. Numerous studies have shown that TP can inhibit obesity and its related metabolism disorders effectively. Meanwhile, it has demonstrated that TP and their derivatives may modulate intestinal micro-ecology. The understanding of the interaction between TP and intestinal microbiota will allow us to better evaluate the contribution of microbial metabolites of TP to anti-obesity activity. This review showed implications for the use of TP as functional food with potential therapeutic utility against obesity by modulating intestinal microbiota, contributing to the improvement of human health. © 2019 Society of Chemical Industry.


Asunto(s)
Fármacos Antiobesidad/metabolismo , Obesidad/metabolismo , Obesidad/microbiología , Polifenoles/metabolismo , Té/metabolismo , Animales , Fármacos Antiobesidad/análisis , Camellia sinensis/química , Camellia sinensis/metabolismo , Microbioma Gastrointestinal , Humanos , Polifenoles/análisis , Té/química
11.
J Clin Endocrinol Metab ; 105(3)2020 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-31606738

RESUMEN

CONTEXT: Oncostatin M (OSM) plays a key role in inflammation, but its regulation and function during obesity is not fully understood. OBJECTIVE: The aim of this study was to evaluate the relationship of OSM with the inflammatory state that leads to impaired glucose homeostasis in obesity. We also assessed whether OSM immunoneutralization could revert metabolic disturbances caused by a high-fat diet (HFD) in mice. DESIGN: 28 patients with severe obesity were included and stratified into two groups: (1) glucose levels <100 mg/dL and (2) glucose levels >100 mg/dL. White adipose tissue was obtained to examine OSM gene expression. Human adipocytes were used to evaluate the effect of OSM in the inflammatory response, and HFD-fed C57BL/6J mice were injected with anti-OSM antibody to evaluate its effects. RESULTS: OSM expression was elevated in subcutaneous and visceral fat from patients with obesity and hyperglycemia, and correlated with Glut4 mRNA levels, serum insulin, homeostatic model assessment of insulin resistance, and inflammatory markers. OSM inhibited adipogenesis and induced inflammation in human adipocytes. Finally, OSM receptor knockout mice had increased Glut4 mRNA levels in adipose tissue, and OSM immunoneutralization resulted in a reduction of glucose levels and Ccl2 expression in adipose tissue from HFD-fed mice. CONCLUSIONS: OSM contributes to the inflammatory state during obesity and may be involved in the development of insulin resistance.


Asunto(s)
Glucosa/metabolismo , Homeostasis , Obesidad/metabolismo , Oncostatina M/fisiología , Adipocitos/citología , Adulto , Animales , Femenino , Transportador de Glucosa de Tipo 4/genética , Humanos , Resistencia a la Insulina , Masculino , Ratones , Ratones Endogámicos C57BL , Persona de Mediana Edad , Receptores de Oncostatina M/fisiología
12.
Curr Diabetes Rev ; 16(2): 95-103, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31267874

RESUMEN

BACKGROUND: Adiponectin is an adipocyte-derived cytokine closely associated with obesity, altered body adipose tissue distribution, insulin resistance, and cardiovascular diseases. INTRODUCTION: Evidence from animal and human studies demonstrate that adiponectin plays an important role in the regulation of glucose and lipid metabolism. Adiponectin increases insulin sensitivity and improves systemic lipid metabolism. Although research efforts on adiponectin mostly aim towards its endocrine functions, this adipocyte-derived molecule also has profound autocrine and paracrine functions. CONCLUSION: In this review, our aim is to discuss the role of adiponectin in maintaining metabolic homeostasis and its association with cardiovascular health. The proper identification of these roles is of great importance, which has the potential to identify a wealth of novel targets for the treatment of diabetes and related cardio-metabolic diseases.


Asunto(s)
Adiponectina/fisiología , Homeostasis/fisiología , Tejido Adiposo/metabolismo , Animales , Enfermedades Cardiovasculares/metabolismo , Comunicación Celular/fisiología , Sistema Nervioso Central/metabolismo , Diabetes Mellitus/metabolismo , Metabolismo Energético/fisiología , Glucosa/metabolismo , Humanos , Resistencia a la Insulina/fisiología , Células Secretoras de Insulina/metabolismo , Metabolismo de los Lípidos/fisiología , Obesidad/metabolismo
13.
Cell Mol Life Sci ; 77(1): 129-147, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31363816

RESUMEN

Obesity is an endemic pathophysiological condition and a comorbidity associated with hypercholesterolemia, hypertension, cardiovascular disease, type 2 diabetes mellitus, and cancer. The adipose tissue of obese subjects shows hypertrophic adipocytes, adipocyte hyperplasia, and chronic low-grade inflammation. S100 proteins are Ca2+-binding proteins exclusively expressed in vertebrates in a cell-specific manner. They have been implicated in the regulation of a variety of functions acting as intracellular Ca2+ sensors transducing the Ca2+ signal and extracellular factors affecting cellular activity via ligation of a battery of membrane receptors. Certain S100 proteins, namely S100A4, the S100A8/S100A9 heterodimer and S100B, have been implicated in the pathophysiology of obesity-promoting macrophage-based inflammation via toll-like receptor 4 and/or receptor for advanced glycation end-products ligation. Also, serum levels of S100A4, S100A8/S100A9, S100A12, and S100B correlate with insulin resistance/type 2 diabetes, metabolic risk score, and fat cell size. Yet, secreted S100B appears to exert neurotrophic effects on sympathetic fibers in brown adipose tissue contributing to the larger sympathetic innervation of this latter relative to white adipose tissue. In the present review we first briefly introduce S100 proteins and then critically examine their role(s) in adipose tissue and obesity.


Asunto(s)
Tejido Adiposo/metabolismo , Obesidad/metabolismo , Proteínas S100/metabolismo , Tejido Adiposo/fisiopatología , Animales , Citocinas/análisis , Citocinas/metabolismo , Humanos , Inflamación/complicaciones , Inflamación/metabolismo , Inflamación/fisiopatología , Macrófagos/metabolismo , Macrófagos/patología , Obesidad/complicaciones , Obesidad/fisiopatología , Proteínas S100/análisis
14.
J Clin Endocrinol Metab ; 105(3)2020 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-31652310

RESUMEN

CONTEXT: Obesity-related insulin resistance (OIR) is one of the main contributors to type 2 diabetes and other metabolic diseases. Protein kinases are implicated in insulin signaling and glucose metabolism. Molecular mechanisms underlying OIR involving global kinase activities remain incompletely understood. OBJECTIVE: To investigate abnormal kinase activity associated with OIR in human skeletal muscle. DESIGN: Utilization of stable isotopic labeling-based quantitative proteomics combined with affinity-based active enzyme probes to profile in vivo kinase activity in skeletal muscle from lean control (Lean) and OIR participants. PARTICIPANTS: A total of 16 nondiabetic adults, 8 Lean and 8 with OIR, underwent hyperinsulinemic-euglycemic clamp with muscle biopsy. RESULTS: We identified the first active kinome, comprising 54 active protein kinases, in human skeletal muscle. The activities of 23 kinases were different in OIR muscle compared with Lean muscle (11 hyper- and 12 hypo-active), while their protein abundance was the same between the 2 groups. The activities of multiple kinases involved in adenosine monophosphate-activated protein kinase (AMPK) and p38 signaling were lower in OIR compared with Lean. On the contrary, multiple kinases in the c-Jun N-terminal kinase (JNK) signaling pathway exhibited higher activity in OIR vs Lean. The kinase-substrate-prediction based on experimental data further confirmed a potential downregulation of insulin signaling (eg, inhibited phosphorylation of insulin receptor substrate-1 and AKT1/2). CONCLUSIONS: These findings provide a global view of the kinome activity in OIR and Lean muscle, pinpoint novel specific impairment in kinase activities in signaling pathways important for skeletal muscle insulin resistance, and may provide potential drug targets (ie, abnormal kinase activities) to prevent and/or reverse skeletal muscle insulin resistance in humans.


Asunto(s)
Resistencia a la Insulina , Músculo Esquelético/enzimología , Obesidad/metabolismo , Proteínas Quinasas/fisiología , Proteoma , Proteínas Quinasas Activadas por AMP/fisiología , Adulto , Femenino , Humanos , Masculino , Transducción de Señal/fisiología , Proteínas Quinasas p38 Activadas por Mitógenos/fisiología
15.
Cell Mol Life Sci ; 77(1): 115-128, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31352534

RESUMEN

Adipose tissue is located in discrete depots that are differentially associated with elevated risk of metabolic complications, with fat accretion in visceral depots being most detrimental to metabolic health. Currently, the regulation of specific adipose depot expansion, by adipocyte hypertrophy and hyperplasia and consequently fat distribution, is not well understood. However, a growing body of evidence from in vitro investigations indicates that mature adipocytes secrete factors that modulate the proliferation and differentiation of progenitor, adipose-derived stem cells (ADSCs). It is therefore plausible that endocrine communication between adipocytes and ADSCs located in different depots influences fat distribution, and may therefore contribute to the adverse health outcomes associated with visceral adiposity. This review will explore the available evidence of paracrine and endocrine crosstalk between mature adipocytes and ADSCs that affects adipogenesis, as a better understanding of the regulatory roles of the extracellular signalling mechanisms within- and between adipose depots may profoundly change the way we view adipose tissue growth in obesity and related comorbidities.


Asunto(s)
Adipocitos/citología , Adipogénesis , Células Madre/citología , Adipocitos/metabolismo , Animales , Comunicación Celular , Humanos , Obesidad/metabolismo , Comunicación Paracrina , Transducción de Señal , Células Madre/metabolismo
16.
Food Chem Toxicol ; 135: 110982, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-31747621

RESUMEN

With epidemic of obesity, it affects aspects of female reproduction. Genistein could ameliorate obesity in people and animals, but might exert adverse effects on the female reproductive system. To evaluate the effects of fetal and neonatal genistein exposure on the ovarian health of F1 obese female mice with obesity induced by high-fat diet after weaning, we simulated a diet-induced obesity model to observe and determine biological effects of genistein exposure on the ovarian follicle of overfed female mice. Results showed that F1 female mice with obesity induced by high-fat diet significantly prolonged the estrus cycle, disrupted sex hormonal balance and ovarian follicle development after they were exposed to 25 mg/kg b.w./day of genistein during the fetal and neonatal stages. Genistein significantly up-regulated the ovarian mRNA expression of estrogen receptor beta in F1 obese female mice, and high-fat diet influenced the ovarian mRNA expression of estrogen receptor alpha, luteinizing hormone receptor and follicle-stimulating hormone receptor. Hence, genistein exposure from the fetal stage might increase the risk of reproductive diseases in obese females in later life. Thus, the long-term risks of genistein to obese females should be thoroughly assessed.


Asunto(s)
Dieta Alta en Grasa , Genisteína/efectos adversos , Obesidad/tratamiento farmacológico , Folículo Ovárico/efectos de los fármacos , Animales , Animales Recién Nacidos , Estradiol/metabolismo , Receptor beta de Estrógeno/genética , Ciclo Estral/efectos de los fármacos , Femenino , Feto/efectos de los fármacos , Hormona Folículo Estimulante/metabolismo , Expresión Génica/efectos de los fármacos , Hormona Luteinizante/metabolismo , Ratones Endogámicos ICR , Obesidad/metabolismo , Folículo Ovárico/embriología , Folículo Ovárico/patología , Embarazo , ARN Mensajero/metabolismo
17.
J Agric Food Chem ; 68(1): 4-16, 2020 Jan 08.
Artículo en Inglés | MEDLINE | ID: mdl-31829005

RESUMEN

Obesity has an important influence on health conditions, causing a multitude of complications and comorbidities, and drug therapy is considered to be one of the treatment strategies. Nowadays, there is increasing interest in the study of intestinal microbiota regulation of obesity; also, an increasing number of agricultural and sideline products have been found to have anti-obesity potential. In the present review, we summarize an overview of current known and potential anti-obesity oligosaccharides and their molecular structures. We describe their anti-obesity potential activity and the molecular structure associated with this activity, the regulation of intestinal microbiota composition and its mechanism of action, including regulation of the short-chain fatty acid (SCFA) pathway and altering bile acid (BA) pathway. This review will provide new ideas for us to develop new anti-obesity functional foods.


Asunto(s)
Fármacos Antiobesidad/administración & dosificación , Obesidad/tratamiento farmacológico , Oligosacáridos/administración & dosificación , Animales , Fármacos Antiobesidad/química , Bacterias/clasificación , Bacterias/genética , Bacterias/aislamiento & purificación , Bacterias/metabolismo , Ácidos Grasos Volátiles/metabolismo , Microbioma Gastrointestinal , Humanos , Obesidad/metabolismo , Obesidad/microbiología , Oligosacáridos/química , Prebióticos/administración & dosificación , Prebióticos/análisis
18.
J Agric Food Chem ; 68(1): 33-47, 2020 Jan 08.
Artículo en Inglés | MEDLINE | ID: mdl-31829012

RESUMEN

Obesity is caused by an imbalance of energy intake and expenditure. It is characterized by a higher accumulation of body fat with a chronic low-grade inflammation. Many reports have shown that gut microbiota in the host plays a pivotal role in mediating the interaction between consumption of a high-fat diet (HFD) and onset of obesity. Accumulative evidence has suggested that the changes in the composition of gut microbiota may affect the host's energy homeostasis, systemic inflammation, lipid metabolism, and insulin sensitivity. As one of the major components in human diet, polyphenols have demonstrated to be capable of modulating the composition of gut microbiota and reducing the HFD-induced obesity. The present review summarizes the findings of recent studies on dietary polyphenols regarding their metabolism and interaction with bacteria in the intestine as well as the underlying mechanisms by which they modulate the gut microbiota and alleviate the HFD-induced obesity.


Asunto(s)
Dieta Alta en Grasa/efectos adversos , Microbioma Gastrointestinal , Obesidad/dietoterapia , Obesidad/microbiología , Polifenoles/metabolismo , Animales , Ingestión de Energía , Humanos , Obesidad/metabolismo
19.
Int J Vitam Nutr Res ; 90(1-2): 23-32, 2020 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-30843770

RESUMEN

Type 2 diabetes mellitus is characterized by the inability to regulate blood glucose levels due to insulin resistance, resulting in hyperglycemia and hyperinsulinemia. Research has shown that consuming soy and fiber may protect against type 2 diabetes mellitus. We performed a study to determine whether supplementing diet with soy extract (0.5% weight of diet) or fiber (as red wheat bran; 11.4% weight of diet) would decrease serum insulin and blood glucose levels in a pre-diabetic/metabolic syndrome animal model. In our study, female obese Zucker rats were fed either a control diet (n = 8) or control diet supplemented with either soy extract (n = 7) or red wheat bran (n = 8) for seven weeks. Compared to rats consuming control diet, rats fed treatment diets had significantly lower (p-value < 0.05) fasting serum insulin (control = 19.34±1.6; soy extract = 11.1±1.54; red wheat bran = 12.4±1.11) and homeostatic model assessment of insulin resistance values (control = 2.16±0.22; soy extract = 1.22±0.21; red wheat bran = 1.54±0.16). Non-fasted blood glucose was also significantly lower (p-value < 0.05) in rats fed treatment diets compared to rats consuming control diet at weeks four (control = 102.63±5.67; soy extract = 80.14±2.13; red wheat bran = 82.63±3.16), six (control = 129.5±10.83; soy extract = 89.14±2.48; red wheat bran = 98.13±3.54), and seven (control = 122.25±8.95; soy extract = 89.14±4.52; red wheat bran = 84.75±4.15). Daily intake of soy extract and red wheat bran may protect against type 2 diabetes mellitus by maintaining normal glucose homeostasis.


Asunto(s)
Diabetes Mellitus Tipo 2 , Glucosa/metabolismo , Insulinas , Animales , Dieta , Fibras de la Dieta/administración & dosificación , Femenino , Glucosa/química , Obesidad/metabolismo , Extractos Vegetales/química , Ratas , Ratas Zucker
20.
Eur J Med Chem ; 187: 111948, 2020 Feb 01.
Artículo en Inglés | MEDLINE | ID: mdl-31877540

RESUMEN

The aldehyde oxidases (AOXs) are a small sub-family of cytosolic molybdo-flavoenzymes, which are structurally conserved proteins and broadly distributed from plants to animals. AOXs play multiple roles in both physiological and pathological processes and AOX inhibition is of increasing significance in the development of novel drugs and therapeutic strategies. This review provides an overview of the evolution and the action mechanism of AOX and the role of each domain. The review provides an update of the polymorphisms in the human AOX. This review also summarises the physiology of AOX in different organs and its role in drug metabolism. The inhibition of AOX is a promising therapeutic treatment for cancer, obesity, aging and amyotrophic lateral sclerosis.


Asunto(s)
Aldehído Oxidasa/antagonistas & inhibidores , Esclerosis Amiotrófica Lateral/tratamiento farmacológico , Antineoplásicos/farmacología , Inhibidores Enzimáticos/farmacología , Neoplasias/tratamiento farmacológico , Fármacos Neuroprotectores/farmacología , Obesidad/tratamiento farmacológico , Aldehído Oxidasa/metabolismo , Esclerosis Amiotrófica Lateral/metabolismo , Animales , Antineoplásicos/química , Inhibidores Enzimáticos/química , Humanos , Neoplasias/metabolismo , Fármacos Neuroprotectores/química , Obesidad/metabolismo
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