Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 1.036
Filter
1.
Neuroscience Bulletin ; (6): 809-819, 2022.
Article in English | WPRIM | ID: wpr-939834

ABSTRACT

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease featuring progressive cognitive impairment. Although the etiology of late-onset AD remains unclear, the close association of AD with apolipoprotein E (APOE), a gene that mainly regulates lipid metabolism, has been firmly established and may shed light on the exploration of AD pathogenesis and therapy. However, various confounding factors interfere with the APOE-related AD risk, raising questions about our comprehension of the clinical findings concerning APOE. In this review, we summarize the most debated factors interacting with the APOE genotype and AD pathogenesis, depict the extent to which these factors relate to APOE-dependent AD risk, and discuss the possible underlying mechanisms.


Subject(s)
Alzheimer Disease/pathology , Apolipoprotein E4/genetics , Apolipoproteins E/genetics , Genotype , Humans , Lipid Metabolism , Neurodegenerative Diseases , Risk Factors
2.
Article in English | WPRIM | ID: wpr-939828

ABSTRACT

Superchilling is an emerging technology for meat preservation; however, the temperature changes during the process have been commonly ignored. Thus, the effects of temperature fluctuations on meat quality during superchilling are yet to be evaluated. In our study, pork loins and salmon fillets were stored for several days (0, 8, 15, 23, and 30 d) under different temperature fluctuations based on -3.5 ℃ as the target temperature. The results showed that after 15 d of superchilling storage, the values of total volatile basic nitrogen, total viable count, and lipid oxidation were significantly (P<0.05) altered in the ±2.0 ℃ fluctuation group compared with the constant temperature group. On the contrary, there was no significant difference in these parameters between the ±1.0 ℃ fluctuation group and the constant temperature group after 30 d of storage. In addition, irregular temperature changes significantly accelerated the modulation of various indicators. In brief, temperature fluctuations and irregular temperature changes accelerated the destruction of muscle structural integrity, increased the water loss, gradually widened the water loss channels, and thereby reduced the edibility by accelerating the spoilage of meat.


Subject(s)
Animals , Lipid Metabolism , Pork Meat , Red Meat , Salmon , Swine , Temperature
3.
Article in English | WPRIM | ID: wpr-939812

ABSTRACT

Renal fibrosis is a common and irreversible pathological feature of end-stage renal disease caused by multiple etiologies. The role of inflammation in renal fibrosis tissue has been generally accepted. The latest view is that fatty acid metabolism disorder contributes to renal fibrosis. peroxisome proliferator activated receptor-gamma coactivator 1α (PGC1α) plays a key role in fatty acid metabolism, regulating fatty acid uptake and oxidized protein synthesis, preventing the accumulation of lipid in the cytoplasm, and maintaining a dynamic balanced state of intracellular lipid. In multiple animal models of renal fibrosis caused by acute or chronic kidney disease, or even age-related kidney disease, almost all of the kidney specimens show the down-regulation of PGC1α. Upregulation of PGC1α can reduce the degree of renal fibrosis in animal models, and PGC1α knockout animals exhibit severe renal fibrosis. Studies have demonstrated that AMP-activated protein kinase (AMPK), MAPK, Notch, tumor necrosis factor-like weak inducer of apoptosis (TWEAK), epidermal growth factor receptor (EGFR), non-coding RNA (ncRNAs), liver kinase B1 (LKB1), hairy and enhancer of split 1 (Hes1), and other pathways regulate the expression of PGC1α and affect fatty acid metabolism. But some of these pathways interact with each other, and the effect of the integrated pathway on renal fibrosis is not clear.


Subject(s)
Animals , Fatty Acids , Fibrosis , Lipid Metabolism , Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism , Renal Insufficiency, Chronic
4.
Acta Physiologica Sinica ; (6): 443-460, 2022.
Article in Chinese | WPRIM | ID: wpr-939579

ABSTRACT

The mammalian internal circadian clock system has been evolved to adapt to the diurnal changes in the internal and external environment of the organism to regulate diverse physiological functions, such as the sleep-wake cycle and feeding rhythm, thereby coordinating the rhythmic changes of energy demand and nutrition supply in each diurnal cycle. The circadian clock regulates glucose metabolism, lipid metabolism, and hormones secretion in diverse tissues and organs, including the liver, skeletal muscle, pancreas, heart, and vessels. As a special "organ" of the host, the gut microbiota, together with the intestinal microenvironment (tissues, cells, and metabolites) in a co-evolutionary process, constitutes a micro-ecosystem and plays an important role in the process of nutrient digestion and absorption in the intestine of the host. In recent years, accumulating evidence indicates that the compositions, quantities, colonization, and functional activities of the gut microbiota exhibit significant circadian variations, which are closely related to the changes of various physiological functions under the regulation of host circadian clock system. In addition, several studies have shown that the gut microbiota can produce many important metabolites such as the short-chain fatty acids through the degradation of indigestive dietary fibers. A portion of gut microbiota-derived metabolites can regulate the circadian clock system and metabolism of the host. This article mainly discusses the interaction between the host circadian clock system and the gut microbiota, and highlights its influence on energy metabolism of the host, providing a novel clues and thought for the prevention and treatment of metabolic diseases.


Subject(s)
Animals , Circadian Clocks/physiology , Circadian Rhythm/physiology , Ecosystem , Energy Metabolism , Gastrointestinal Microbiome/physiology , Lipid Metabolism/physiology , Mammals
5.
Article in Chinese | WPRIM | ID: wpr-935736

ABSTRACT

Objective: To investigate the effect of pesticides and herbicides on lipid metabolism. Methods: In November 2020, Based on the data of the national health and Nutrition Survey (NHANES) (2011-2014) , select the population aged 20~65 who have demographic information, pesticide use and data of four lipid metabolism indicators [total cholesterol (TC) , triglyceride (TG) , high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDLC) ] (n=3039) . The subjects were divided into insecticide group (320 people) and non insecticide group (2719) according to the use of insecticides, and herbicide group (156 people) and non herbicide group according to the use of herbicides. Results: Among the 3039 subjects, the males and female were 1509 (49.7%) and 1530 (50.3%) respectively. The males age was (39.7±12.0) years and the females age was (40.2±12.0) years The concentration of HDLC in the NHANES (55.4±15.0) mg/dl was lower than that of (58.2±14.2) mg/dL in the non herbicide group (P<0.05) (b=-0.044, P<0.05) . The results showed that the use of herbicides was related to the decrease of HDLC and the increase of LDLC and LDLC/HDLC in female population (b=-0.050, 0.062, 0.067, all P<0.05) . Conclusion: Herbicide exposure can cause the change of lipid metabolism, and the effect on female population is more obvious.


Subject(s)
Adult , Cholesterol, HDL , Cholesterol, LDL , Female , Humans , Lipid Metabolism , Male , Middle Aged , Nutrition Surveys , Pesticides , Young Adult
6.
Article in Chinese | WPRIM | ID: wpr-935291

ABSTRACT

Objective: To analyze the effect of psychological suggestion combined with rational food restriction therapy on blood glucose, lipid metabolism and mental resilience in patients with diabetes. Methods: Patients with diabetes admitted to the Third Hospital of Nanchang from January 2020 to August 2020 were divided into the control group and the intervention group with randomized controlled and single blind methods. The control group was treated with routine dietary guidance and health education, and the intervention group was treated with psychological suggestion combined with rational diet therapy on the basis of the control group. Both groups were treated for 3 months. Blood glucose, lipid metabolism, mental resilience and quality of life were compared between the two groups at baseline and after 3-month intervention. Differences between groups and within groups were analyzed by t test and χ2 test. Results: 100 patients in the control group and 81 patients in the intervention group completed 3-month intervention. After 3-month intervention, the levels of glycosylated hemoglobin, fasting blood glucose, 2-hour postprandial blood glucose, low-density lipoprotein cholesterol and triglyceride in both groups were lower than those before intervention. The levels of these indicators in intervention group were lower than those in control group (P<0.05). However, the levels of high-density lipoprotein cholesterol and the scores of tenacity, self-reliance, optimism, role function, emotional function, social function, physical function and cognitive function in both groups were higher than those before intervention. These indicators in intervention group were higher than those in control group (P<0.05). Conclusion: Psychological suggestion combined with rational food restriction therapy could effectively improve the glucose and lipid metabolism, mental resilience, and quality of life among patients with diabetes.


Subject(s)
Blood Glucose/metabolism , Diabetes Mellitus, Type 2 , Humans , Lipid Metabolism , Quality of Life , Single-Blind Method
7.
Article in Chinese | WPRIM | ID: wpr-928057

ABSTRACT

This paper aims to study the effect of Xiangqin Jiere Granules(XQ) on lipid metabolism and chronic inflammation in different obesity model mice. The monosodium glutamate(MSG) obese mouse model was established by subcutaneous injection of MSG in newborn mice, and the high fat diet(HFD) obese mouse model was established by feeding adult mice with HFD. The normal mice were assigned into the control group; the MSG obese mice were assigned into MSG model group, XQ4.5 group(Xiangqin Jiere Granu-les, 4.5 g·kg~(-1)), XQ22.5 group(Xiangqin Jiere Granules, 22.5 g·kg~(-1)); the HFD obese mice were assigned into HFD model group, XQ4.5 group, and XQ22.5 group. The mice were intragastrically administrated with saline or XQ for 5 weeks. After that, the body weight, visceral fat mass, liver and thymus weight, and the organ indexes in each group were measured. The levels of triglyceride(TG), total cholesterol(TC), and low-density lipoprotein cholesterol(LDL-c) in serum and liver tissue were detected by the kits. The mRNA expression levels of acetyl CoA carboxylase 1(ACC1), fatty acid synthetase(FAS), diacylgycerol acyltransferase 1(DGAT1) and hepatic lipase(HTGL) involved in lipid metabolism in mouse liver tissue were detected by quantitative real-time PCR(qPCR). The protein levels of tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in serum were detected by ELISA, and the mRNA levels of TNF-α and IL-6 in liver tissue were detected by qPCR. Compared with the control group, MSG and HFD mice showed increased body weight, abdominal circumference, Lee index and visceral fat mass as well as elevated levels of TG, TC, and LDL-c in serum. The model mice had up-regulated gene levels of ACC1, FAS and DGAT1 while down-regulated gene level of HTGL in the liver. Furthermore, the mRNA and protein levels of IL-6 increased in the model mice. Compared with the model mice, XQ treatment decreased the body weight, abdominal circumference, Lee index, and visceral fat mass, lowered the levels of TG, TC, and LDL-c in se-rum, down-regulated the gene levels of ACC1, FAS, and DGAT1 in liver tissue, up-regulated the gene level of HTGL, and down-regulated the mRNA and protein levels of IL-6. To sum up, XQ has good therapeutic effect on different obesity model mice. It can improve lipid metabolism and reduce fat accumulation in obese mice by regulating the enzymes involved in lipid metabolism, and alleviate obesity-related chronic low-grade inflammation.


Subject(s)
Animals , Inflammation/metabolism , Lipid Metabolism , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity/genetics
8.
Article in English | WPRIM | ID: wpr-927639

ABSTRACT

OBJECTIVE@#This study aimed to investigate the effects of caprylic acid (C8:0) on lipid metabolism and inflammation, and examine the mechanisms underlying these effects in mice and cells.@*METHODS@#Fifty-six 6-week-old male C57BL/6J mice were randomly allocated to four groups fed a high-fat diet (HFD) without or with 2% C8:0, palmitic acid (C16:0) or eicosapentaenoic acid (EPA). RAW246.7 cells were randomly divided into five groups: normal, lipopolysaccharide (LPS), LPS+C8:0, LPS+EPA and LPS+cAMP. The serum lipid profiles, inflammatory biomolecules, and ABCA1 and JAK2/STAT3 mRNA and protein expression were measured.@*RESULTS@#C8:0 decreased TC and LDL-C, and increased the HDL-C/LDL-C ratio after injection of LPS. Without LPS, it decreased TC in mice ( P < 0.05). Moreover, C8:0 decreased the inflammatory response after LPS treatment in both mice and cells ( P < 0.05). Mechanistic investigations in C57BL/6J mouse aortas after injection of LPS indicated that C8:0 resulted in higher ABCA1 and JAK2/STAT3 expression than that with HFD, C16:0 and EPA, and resulted in lower TNF-α, NF-κB mRNA expression than that with HFD ( P < 0.05). In RAW 264.7 cells, C8:0 resulted in lower expression of pNF-κBP65 than that in the LPS group, and higher protein expression of ABCA1, p-JAK2 and p-STAT3 than that in the LPS and LPS+cAMP groups ( P < 0.05).@*CONCLUSION@#Our studies demonstrated that C8:0 may play an important role in lipid metabolism and the inflammatory response, and the mechanism may be associated with ABCA1 and the p-JAK2/p-STAT3 signaling pathway.


Subject(s)
ATP Binding Cassette Transporter 1/immunology , Animals , Caprylates/chemistry , Cholesterol/metabolism , Diet, High-Fat/adverse effects , Humans , Inflammation/metabolism , Janus Kinase 2/immunology , Lipid Metabolism/drug effects , Macrophages/immunology , Male , Mice , Mice, Inbred C57BL , STAT3 Transcription Factor/immunology , Signal Transduction
9.
Acta Physiologica Sinica ; (6): 309-319, 2022.
Article in Chinese | WPRIM | ID: wpr-927607

ABSTRACT

Lipophagy is a kind of selective autophagy, which can selectively identify and degrade lipid droplets and plays an important role in regulating cellular lipid metabolism and maintaining intracellular lipid homeostasis. Exercise can induce lipophagy and it is also an effective means of reducing body fat. In this review, we summarized the relationship between exercise and lipophagy in the liver, pancreas, adipose tissue, and the possible molecular mechanisms to provide a new clue for the prevention and treatment of fatty liver, obesity and other related metabolic diseases by exercise.


Subject(s)
Autophagy/physiology , Humans , Lipid Droplets/metabolism , Lipid Metabolism/physiology , Liver , Metabolic Diseases/metabolism
10.
Acta Physiologica Sinica ; (6): 301-308, 2022.
Article in Chinese | WPRIM | ID: wpr-927606

ABSTRACT

Nogo-B receptor (NgBR) is a specific receptor of Nogo-B, a member of reticulon 4 protein family. It is widely expressed in many tissues and mainly located in cell membrane and endoplasmic reticulum. Previous studies have revealed that NgBR is involved in a variety of physiological and pathophysiological processes, such as dolichol synthesis, lipid metabolism, cholesterol trafficking, insulin resistance, vascular remodeling and angiogenesis, tumorigenesis and nervous system diseases. Further studies on the molecular characteristics and biological function of NgBR might be of great significance to understand its role in diverse diseases and provide possible clinical strategies for the treatment of diseases.


Subject(s)
Carrier Proteins/metabolism , Endoplasmic Reticulum/metabolism , Lipid Metabolism , Nogo Proteins/metabolism , Receptors, Cell Surface/metabolism
12.
Article in Chinese | WPRIM | ID: wpr-936366

ABSTRACT

OBJECTIVE@#To investigate the changes of tetraspanin 8 (TSPAN8) expression levels and its role in lipid metabolism during the development of non-alcoholic fatty liver disease (NAFLD).@*METHODS@#Thirty male C57BL/6J mice were randomly divided into normal diet group and high-fat diet (HFD) group (n=15), and after feeding for 1, 3, and 6 months, the expression levels of TSPAN8 in the liver tissues of the mice were detected with Western blotting. In a HepG2 cell model of NAFLD induced by free fatty acids (FFA), the effect of TSPAN8 overexpression on lipid accumulation was examined using Oil Red O staining and an automated biochemical analyzer, and the mRNA expressions of the key genes involved in lipid metabolism were detected using qRT-PCR.@*RESULTS@#Western blotting showed that compared with that in mice with normal feeding, the expression of TSPAN8 was significantly decreased in the liver tissues of mice with HFD feeding for 3 and 6 months (P < 0.05). In HepG2 cells, treatment with FFA significantly decreased the expression of TSPAN8 at both the mRNA and protein levels (P < 0.01). TSPAN8 overexpression in FFA-treated cells showed significantly lowered intracellular triglyceride levels (P < 0.001) and obviously reduced mRNA expression of fatty acid transport protein 5 (FATP5) (P < 0.01). The expression of FATP5 was significantly increased in FFA-treated cells as compared with the control cells (P < 0.001).@*CONCLUSION@#TSPAN8 is involved in lipid metabolism in NAFLD, and overexpression of TSPAN8 may inhibit cellular lipid deposition by reducing the expression of FATP5.


Subject(s)
Animals , Diet, High-Fat/adverse effects , Fatty Acids, Nonesterified , Lipid Metabolism , Liver/metabolism , Male , Mice , Mice, Inbred C57BL , Non-alcoholic Fatty Liver Disease/metabolism , RNA, Messenger/metabolism
13.
Article in English | WPRIM | ID: wpr-929001

ABSTRACT

OBJECTIVES@#Perfluorooctanoic acid (PFOA) can cause lipid metabolism disorders in animal body and affect the lipolysis and synthesis of fatty acids. Peroxisome proliferators-activated receptor (PPAR) plays an extremely important role in this process. This study aims to explore the effects of PFOA on liver lipid metabolism disorders in Sprague Dewley (SD) rats and the expression of PPAR.@*METHODS@#A total of 40 male SD rats were randomly divided into 4 groups (n=10 in each group): a control group (ddH2O), a low-dose PFOA group [PFOA 1.25 mg/(kg·d)], a middle-dose PFOA group [PFOA 5.00 mg/(kg·d)], and a high-dose PFOA group [PFOA 20.00 mg/(kg·d)]. The rats were fed with normal diet, and PFOA exposure were performed by oral gavage for 14 days, and the rats were observed, weighted and recorded every day during the exposure. After the exposure, the blood was collected, and the livers were quickly stripped after the rats were killed. Part of the liver tissues were fixed in 4% paraformaldehyde for periodic acid-schiff (PAS) staining; the contents of HDLC, LDLC, TG, TC in serum and liver tissues, as well as the activities of their related enzymes were assayed; The expression levels of cyclic adenosine monophosphate-response element binding protein (Cbp), general control of amino acid synthesis 5-like 2 (Gcn5L2), peroxidation peroxisome proliferation factor activated receptor γ (PPAR), silent information regulator 1 (Sirt1) and human retinoid X receptor alpha 2 (Rxrα2) ) were detected by Western blotting.@*RESULTS@#After 14 days of PFOA exposure, the PAS staining positive particles in the cytoplasm and nucleus of SD rats in the medium and high dose groups were significantly reduced compared with the control group. The serum levels of LDLC and TC in the low-dose and middle-dose groups were significantly reduced compared with the control group (all P<0.05), while the high-dose group showed an increasing tendency, without siginificant difference (P>0.05), there was no significant difference in HDLC and TG (both P>0.05). The activities of alkaline phosphatase (AKP) and alanine aminotransferase (ALT) were increased significantly (both P<0.05) compared with control group; the ratio of ALT/aspartate aminotransferase (AST) in the high-dose group was increased significantly (P<0.05), there was no significant difference in LDH and TG (both P>0.05); the HDLC content in the liver tissues in the high-dose group was significantly reduced, compared with the control group (P<0.05); the TC contents in the liver tissues in the low, medium and high-dose groups were significantly increased (all P<0.05), there was no significant difference in LDLC and TG (both P>0.05); the AKP activity in the livers in the medium and high-dose groups was significantly increased (both P<0.05), there was no siginificant difference in LDH, ALT, and the ratio of ALT/AST (all P>0.05); the protein expression levels of Ppar γ, Cbp and Rxrα2 in the liver in the high dose groups were significantly down-regulated compared with the control group (all P<0.05), while the protein expression levels of Sirt1 were significantly up-regulated (all P<0.05).@*CONCLUSIONS@#PFOA exposure can cause lipid metabolism disorder and glycogen reduction in SD rat livers, which may be related to the activation of Sirt1 and inhibition of Ppar γ expression, leading to affecting the normal metabolism of fatty acids and promoting glycolysis.


Subject(s)
Animals , Caprylates , Fatty Acids/pharmacology , Fluorocarbons , Lipid Metabolism , Lipid Metabolism Disorders/metabolism , Liver/metabolism , Male , PPAR gamma , Rats , Rats, Sprague-Dawley , Sirtuin 1/metabolism
14.
Arch. latinoam. nutr ; 71(4): 261-269, dic. 2021. tab
Article in English | LILACS, LIVECS | ID: biblio-1355151

ABSTRACT

Insulin resistance is a pathological entity that can lead to alterations in lipid metabolism and can increase cardiovascular risk. Objective. The aim of this study was to assess the influence of different sociodemographic variables such as age, sex and social class and healthy habits such as smoking, physical activity and adherence to the Mediterranean diet on the cardiometabolic profile of Spanish workers. Material and methods. A descriptive, cross-sectional study was carried out in 1457 Spanish workers in an attempt to evaluate the effect of healthy habits (physical exercise determined with the IPAQ questionnaire, Mediterranean diet and tobacco consumption) and sociodemographic variables (age, sex and social class) on the values of different insulin resistance scales. Results. The progressive increase in the level of physical activity and high adherence to the Mediterranean diet achieved an improvement in the mean values and in the prevalence of elevated values in all the insulin resistance scales analyzed in this study. Age over 50 years and belonging to the least favored social classes (social classes II-III) were the variables that increased the risk of presenting insulin resistance. Male sex also increased the risk of presenting insulin resistance. Conclusions. The different healthy habits such as vigorous physical exercise and high adherence to the Mediterranean diet improve the values of the different scales that assess insulin resistance(AU)


La resistencia a la insulina es una entidad patológica que puede provocar alteraciones en el metabolismo de los lípidos y puede aumentar el riesgo cardiovascular. Objetivo. En este trabajo se pretende valorar la influencia de diferentes variables sociodemográficas como la edad, el sexo y la clase social y hábitos saludables como el consumo de tabaco, la actividad física y la adherencia a la dieta mediterránea en el perfil cardiometabólico de trabajadores españoles. Material y métodos. Se realizó un estudio descriptivo y transversal en 1457 trabajadores españoles intentando evaluar el efecto de los hábitos saludables (ejercicio físico determinado con el cuestionario IPAQ, dieta mediterránea y consumo de tabaco) y las variables sociodemográficas (edad, sexo y clase social) sobre los valores de diferentes escalas de resistencia a la insulina. Resultados. El aumento progresivo del nivel de actividad física y la alta adherencia a la dieta mediterránea consiguieron una mejoría en los valores medios y en la prevalencia de los valores elevados en todas las escalas de resistencia a la insulina analizadas en este estudio. La edad por encima de los 50 años y la pertenencia a las clases sociales menos favorecidas (clases sociales II-III) fueron las variables que aumentaron el riesgo de presentar resistencia a la insulina. El sexo masculino también incrementó el riesgo de presentar resistencia a la insulina. Conclusiones. Los diferentes hábitos saludables como el ejercicio físico vigoroso y la alta adherencia a la dieta mediterránea mejoran los valores de las diferentes escalas que valoran resistencia a la insulina(AU)


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Insulin Resistance , Metabolic Syndrome/complications , Diet, Mediterranean , Lipid Metabolism , Healthy Lifestyle , Cardiometabolic Risk Factors , Social Class , Weights and Measures , Exercise , Nutrition Assessment , Abdominal Circumference , Feeding Behavior
15.
Arch. argent. pediatr ; 119(2): 114-122, abril 2021. tab, ilus
Article in English, Spanish | LILACS, BINACIS | ID: biblio-1151867

ABSTRACT

Introducción. La obesidad infantil puede causar hiperlipidemia y esteatosis hepática y complicaciones crónicas. Nuestro objetivo fue evaluar la relación entre el espesor de la grasa subcutánea abdominal (GSA) y la esteatosis hepática, las transaminasas y los lípidos séricos en niños obesos.Población y métodos. Estudio retrospectivo en niños (4-18 años) que acudieron a los consultorios externos. Se evaluaron las asociaciones entre el espesor de la GSA mediante ecografía y la esteatosis hepática, alanina aminotransferasa (ALT), aspartato aminotransferasa (AST) y el perfil lipídico sérico.Resultados. Se identificaron 95 niños con esteatosis hepática; el grado 1 fue el más frecuente (73,6 %, n: 70), seguido del grado 2 (21,1 %) y del 3 (5,3 %). El espesor medio (en mm) de la GSA de línea media y flancos fue 38,48 ± 11,53 y 20,91 ± 8,00 en grado 1; 41,23 ± 10,03 y 19,84 ± 6,75 en grado 2, y 63,12 ± 12,08 y 23,22 ± 5,92 en grado 3, respectivamente. El espesor de la GSA de línea media y flancos se correlacionó positivamente con triglicéridos en grado 3; el espesor de la GSA de línea media se correlacionó con el índice de masa corporal, colesterol total, colesterol LDL y AST (r: 0,9; p: 0,037; r: 0,648; p: 0,001; r: 0,387; p: 0,001; r: 0,406; p: 0,001; r: 0,463; p: 0,001; respectivamente) en grado 1.Conclusión. El espesor de la GSA mediante ecografía puede predecir hiperlipidemia en niños obesos con esteatosis hepática de grado 3 e hipercolesterolemia en grado 1.


Introduction. Childhood obesity can cause hyperlipidemia and hepatic steatosis at early age and chronic disease complications in adult life. We aimed to evaluate the relationship between abdominal subcutaneous fat thickness (ASFT) and hepatic steatosis, serum lipid and transaminase levels in obese children.Population and methods. A retrospective study was conducted with children (aged 4-18 years) who presented to outpatient clinic due to obesity. Associations between ASFT as assessed by ultrasonography (US) and hepatic steatosis, alanine transaminase (ALT), aspartate transaminase (AST) and serum lipid profile were evaluated.Results. We identified 95 children, all of which were diagnosed as having hepatic steatosis; the most common type was grade 1 (73.6 %, n: 70), followed by grade 2 (21.1 %) and grade 3 (5.3 %). The mean values of midline and flank ASFT were measured as 38.48 ± 11.53 mm and 20.91 ± 8.00 mm in grade 1; 41.23 ± 10.03 and 19.84 ± 6.75 in grade 2 and 63.12 ± 12.08 and 23.22 ± 5.92 in grade 3 hepatic steatosis, respectively. Midline and flank ASFT correlated positively with triglycerides in grade 3 steatosis, while midline ASFT correlated with body mass index, total cholesterol, low-density lipoprotein cholesterol, and AST (r: 0.9; p: 0.037; r: 0.648, p: 0.001; r: 0.387, p: 0.001; r: 0.406, p: 0.001, r: 0.463, p: 0.001; respectively) in grade 1 steatosis.Conclusion. ASFT as assessed by US may be of predictive value for hyperlipidemia in grade 3 and for hypercholesterolemia in grade 1 hepatic steatosis in obese children.


Subject(s)
Humans , Male , Child, Preschool , Child , Adolescent , Subcutaneous Fat, Abdominal/diagnostic imaging , Pediatric Obesity , Turkey/epidemiology , Retrospective Studies , Lipid Metabolism , Fatty Liver/diagnostic imaging , Transaminases
16.
Arq. ciências saúde UNIPAR ; 25(1): 61-77, jan-abr. 2021.
Article in Portuguese | LILACS | ID: biblio-1151421

ABSTRACT

A obesidade é caracterizada pelo aumento excessivo da gordura corporal e está ligada ao estilo de vida, ao meio ambiente e a genética do indivíduo. O equilíbrio entre ingestão e gasto energético é controlado por mecanismos neurais, hormonais, químicos e genéticos. Estudos sugerem que o gene FTO (Fat mass and obesity associated) atua como regulador primário do acúmulo de gordura corporal, quando associado a SNPs (Single Nucleotide Polymorphism) específicos, predispõe à obesidade. O propósito deste trabalho foi verificar a produção científica, analisar e catalogar os estudos de polimorfismos no gene FTO associados à obesidade e suas comorbidades. A busca por publicações entre 2009 e 2018 foi realizada na base de dados SciELO com a palavra-chave "FTO". Foram encontrados 23 artigos originais dentro dos critérios da pesquisa que correlacionam o FTO à obesidade. O nome do autor principal, país, idioma, ano de publicação, título, objetivo, polimorfismo associado e os resultados dos estudos foram extraídos e organizados para facilitar a tabulação dos dados. Também foram pesquisados os números de citações de cada artigo, utilizando-se a plataforma Google Acadêmico. Embora o Brasil se encontre em primeiro lugar em produção científica para o gene FTO na base de dados prospectada, o número de artigos originais ainda é muito modesto. Assim, os resultados encontrados podem servir de subsídio no delineamento de novas pesquisas sobre os polimorfismos do gene FTO e as causas da obesidade.


Obesity is characterized by the excessive increase in body fat and is correlated to the lifestyle, environment, and also to the genetics of the individual. The balance between energy intake and expenditure is controlled by neural, hormonal, chemical, and genetic mechanisms. Studies suggest that the FTO (fat mass and obesity associated), a gene associated with fat mass, plays a role as a primary regulator of body fat buildup, when associated to specific Single Nucleotide Polymorphisms (SNPs), causing predisposition to obesity. This paper aimed at reviewing, analyzing, and cataloguing the studies on FTO gene polymorphisms associated with obesity and its comorbidities. The search was carried out in SciELO database, checking articles published between 2009 and 2018 using the keyword "FTO". Twenty-three original articles, matching the research criteria, correlating FTO either positively or negatively with obesity, were found. The main author's name, country, language, year of publication, title, objective, associated polymorphism, and the study results were extracted and organized to facilitate data tabulation. The citation numbers for each article were also searched by using the Google Scholar platform. Although Brazil ranks first in scientific production on the FTO gene in the surveyed database, the number of original articles is still very modest. Therefore, the results found in this paper may be used as a basis for the design of new research on the FTO gene polymorphisms and the causes of obesity.


Subject(s)
Polymorphism, Single Nucleotide , Genetics , Obesity/genetics , Satiety Response , Energy Intake/genetics , Body Mass Index , Adipose Tissue , Lipid Metabolism/genetics , Nutrigenomics , Fats , Genotype , Life Style , Metabolism/genetics
17.
Protein & Cell ; (12): 717-733, 2021.
Article in English | WPRIM | ID: wpr-888715

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is spread primary via respiratory droplets and infects the lungs. Currently widely used cell lines and animals are unable to accurately mimic human physiological conditions because of the abnormal status of cell lines (transformed or cancer cells) and species differences between animals and humans. Organoids are stem cell-derived self-organized three-dimensional culture in vitro and model the physiological conditions of natural organs. Here we showed that SARS-CoV-2 infected and extensively replicated in human embryonic stem cells (hESCs)-derived lung organoids, including airway and alveolar organoids which covered the complete infection and spread route for SARS-CoV-2 within lungs. The infected cells were ciliated, club, and alveolar type 2 (AT2) cells, which were sequentially located from the proximal to the distal airway and terminal alveoli, respectively. Additionally, RNA-seq revealed early cell response to virus infection including an unexpected downregulation of the metabolic processes, especially lipid metabolism, in addition to the well-known upregulation of immune response. Further, Remdesivir and a human neutralizing antibody potently inhibited SARS-CoV-2 replication in lung organoids. Therefore, human lung organoids can serve as a pathophysiological model to investigate the underlying mechanism of SARS-CoV-2 infection and to discover and test therapeutic drugs for COVID-19.


Subject(s)
Adenosine Monophosphate/therapeutic use , Alanine/therapeutic use , Alveolar Epithelial Cells/virology , Antibodies, Neutralizing/therapeutic use , COVID-19/virology , Down-Regulation , Drug Discovery , Human Embryonic Stem Cells/metabolism , Humans , Immunity , Lipid Metabolism , Lung/virology , RNA, Viral/metabolism , SARS-CoV-2/physiology , Virus Replication/drug effects
18.
Article in Chinese | WPRIM | ID: wpr-888193

ABSTRACT

As a unicellular organism, Plasmodium displays a panoply of lipid metabolism pathways that are seldom found together in a unicellular organism. These pathways mostly involve the Plasmodium-encoded enzymatic machinery and meet the requirements of membrane synthesis during the rapid cell growth and division throughout the life cycle. Different lipids have varied synthesis and meta-bolism pathways. For example, the major phospholipids are synthesized via CDP-diacylglycerol-dependent pathway in prokaryotes and de novo pathway in eukaryotes, and fatty acids are synthesized mainly via type Ⅱ fatty acid synthesis pathway. The available studies have demonstrated the impacts of artemisinin and its derivatives, the front-line compounds against malaria, on the lipid metabolism of Plasmodium. Therefore, this article reviewed the known lipid metabolism pathways and the effects of artemisinin and its derivatives on these pathways, aiming to deepen the understanding of lipid synthesis and metabolism in Plasmodium and provide a theoretical basis for the research on the mechanisms and drug resistance of artemisinin and other anti-malarial drugs.


Subject(s)
Antimalarials/pharmacology , Artemisinins/therapeutic use , Humans , Lipid Metabolism , Malaria/drug therapy , Plasmodium
19.
Article in Chinese | WPRIM | ID: wpr-888147

ABSTRACT

This study explored the molecular mechanism underlying the Gegen Qinlian Decoction(GQD) promoting the differentiation of brown adipose tissue(BAT) to improve glucose and lipid metabolism disorders in diabetic rats. After the hypoglycemic effect of GQD on diabetic rats induced by high-fat diet combined with a low dose of streptozotocin was confirmed, the total RNA of rat BAT around scapula was extracted. Nuclear transcription genes Prdm16, Pparγc1α, Pparα, Pparγ and Sirt1, BAT marker genes Ucp1, Cidea and Dio2, energy expenditure gene Ampkα2 as well as BAT secretion factors Adpn, Fndc5, Angptl8, IL-6 and Rbp4 were detected by qPCR, then were analyzed by IPA software. Afterward, the total protein from rat BAT was extracted, and PRDM16, PGC1α, PPARγ, PPARα, SIRT1, ChREBP, AMPKα, UCP1, ADPN, NRG4, GLUT1 and GLUT4 were detected by Western blot. The mRNA expression levels of Pparγc1α, Pparα, Pparγ, Ucp1, Cidea, Ampkα2, Dio2, Fndc5, Rbp4 and Angptl8 were significantly increased(P<0.05) and those of Adpn and IL-6 were significantly decreased(P<0.05) in the GQD group compared with the diabetic group. In addition, Sirt1 showed a downward trend(P=0.104), whereas Prdm16 tended to be up-regulated(P=0.182) in the GQD group. IPA canonical pathway analysis and diseases-and-functions analysis suggested that GQD activated PPARα/RXRα and SIRT1 signaling pathways to promote the differentiation of BAT and reduce the excessive lipid accumulation. Moreover, the protein expression levels of PRDM16, PGC1α, PPARα, PPARγ, SIRT1, ChREBP, AMPKα, UCP1, GLUT1, GLUT4 and NRG4 were significantly decreased in the diabetic group(P<0.01), which were elevated after GQD intervention(P<0.05). Unexpectedly, the expression of ADPN protein in the diabetic group was up-regulated(P<0.01) as compared with the control group, which was down-regulated after the administration with GQD(P<0.01). This study indicated that GQD promoted BAT differentiation and maturity to increase energy consumption, which reduced the glucose and lipid metabolism disorders and thereby improved diabetes symptoms.


Subject(s)
Adipose Tissue, Brown , Animals , Diabetes Mellitus, Experimental/genetics , Drugs, Chinese Herbal , Fibronectins , Glucose , Lipid Metabolism , Lipid Metabolism Disorders , Rats
20.
Acta Physiologica Sinica ; (6): 657-664, 2021.
Article in Chinese | WPRIM | ID: wpr-887700

ABSTRACT

Arachidonic acid (AA) is an ω-6 polyunsaturated fatty acid, which mainly exists in the cell membrane in the form of phospholipid. Three major enzymatic pathways including the cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 monooxygenase (CYP450) pathways are involved in AA metabolism leading to the generation of a variety of lipid mediators such as prostaglandins, leukotrienes, hydroxyeicosatetraenoic acids (HETEs) and epoxyeicoastrienoic acids (EETs). These bioactive AA metabolites play an important role in the regulation of many physiological processes including the maintenance of liver glucose and lipid homeostasis. As the central metabolic organ, the liver is essential in metabolism of carbohydrates, lipids and proteins, and its dysfunction is associated with the pathogenesis of many metabolic diseases such as type 2 diabetes mellitus, dyslipidemia and nonalcoholic fatty liver disease (NAFLD). This article aims to provide an overview of the enzymatic pathways of AA and discuss the role of AA-derived lipid mediators in the regulation of hepatic glucose and lipid metabolism and their associations with the pathogenesis of major metabolic disorders.


Subject(s)
Arachidonic Acid/metabolism , Diabetes Mellitus, Type 2 , Glucose/metabolism , Homeostasis , Humans , Lipid Metabolism , Liver
SELECTION OF CITATIONS
SEARCH DETAIL