Adiponectin gene expression and adipocyte diameter: a comparison between epicardial and subcutaneous adipose tissue in men

Bambace, Clara; Telesca, Mariassunta; Zoico, Elena; Sepe, Anna; Olioso, Debora; Rossi, Andrea P.; Corzato, Francesca; Francesco, Vincenzo Di; Mazzucco, Alessandro; Santini, Francesco; Zamboni, Mauro

doi:10.1016/j.carpath.2010.07.005

Cited by 102 publications

(67 citation statements)

References 5 publications

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“…Significant Gene Ontology (GO) terms, which are used to describe shared relationships between sets of genes, revealed that leukocyte migration and immune system processes were significantly enriched terms for genes that were upregulated in large adipocytes (Table 4). Adiponectin mRNA was also found to be negatively associated with the size of isolated adipocytes (Bambace et al, 2011), whereas leptin mRNA was positively associated with adipocyte volume in isolated adipocytes …”

Section: Transcriptomic Differences In Distinct Adipose Morphologiesmentioning

confidence: 93%

Adipose morphology and metabolic disease

Tandon

Wafer

Minchin

2018

Journal of Experimental Biology

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Adipose morphology is defined as the number and size distribution of adipocytes (fat cells) within adipose tissue. Adipose tissue with fewer but larger adipocytes is said to have a 'hypertrophic' morphology, whereas adipose with many adipocytes of a smaller size is said to have a 'hyperplastic' morphology. Hypertrophic adipose morphology is positively associated with insulin resistance, diabetes and cardiovascular disease. By contrast, hyperplastic morphology is associated with improved metabolic parameters. These phenotypic associations suggest that adipose morphology influences risk of cardiometabolic disease. Intriguingly, monozygotic twin studies have determined that adipose morphology is in part determined genetically. Therefore, identifying the genetic regulation of adipose morphology may help us to predict, prevent and ameliorate insulin resistance and associated metabolic diseases. Here, we review the current literature regarding adipose morphology in relation to: (1) metabolic and medical implications; (2) the methods used to assess adipose morphology; and (3) transcriptional differences between morphologies. We further highlight three mechanisms that have been hypothesized to promote adipocyte hypertrophy and thus to regulate adipose morphology.

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Section: Transcriptomic Differences In Distinct Adipose Morphologiesmentioning

confidence: 93%

Adipose morphology and metabolic disease

Tandon

Wafer

Minchin

2018

Journal of Experimental Biology

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“…Some studies showed that subcutaneous abdominal adipocyte area is positively associated with unfavorable metabolic indexes (Imbeault et al 1999). Larger adipocytes release lower amounts of adiponectin (Skurk et al 2007, Bambace et al 2011. Thus, the lower subcutaneous adipocyte area may counterbalance the higher VFM, which could be responsible for hyperglycemia and hypertriglyceridemia, increasing adiponectin production.…”

Section: Adulthood Alterationsmentioning

confidence: 99%

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

Santos-Silva

Oliveira

Pinheiro

et al. 2013

Journal of Endocrinology

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Children from pregnant smokers show more susceptibility to develop obesity in adult life. Previously, we failed to demonstrate a program for obesity in rat offspring only when the mothers were exposed to tobacco smoke during lactation. Here, we studied the short-and long-term effects of smoke exposure (SE) to both dams and their pups during lactation on endocrine and metabolic parameters. For this, we designed an experimental model where nursing rats and their pups were divided into two groups: SE group, exposed to smoke in a cigarette smoking machine (four times/day, from the third to the 21st day of lactation), and group, exposed to filtered air. Pups were killed at 21 and 180 days. At weaning, SE pups showed lower body weight (7%), length (5%), retroperitoneal fat mass (59%), visceral adipocyte area (60%), and higher subcutaneous adipocyte area (95%) with hypoinsulinemia (K29%), hyperthyroxinemia (59%), hypercorticosteronemia (60%), and higher adrenal catecholamine content (C58%). In adulthood, SE offspring showed higher food intake (C10%), body total fat mass (C50%), visceral fat mass (retroperitoneal: 55%; mesenteric: 67%; and epididymal: 55%), and lower subcutaneous adipocyte area (24%) with higher serum glucose (11%), leptin (85%), adiponectin (1.4-fold increase), total triiodothyronine (71%), free thyroxine (57%), TSH (36%), triglycerides (65%), VLDL cholesterol (C66%), and HDL cholesterol (91%) levels and lower corticosteronemia (41%) and adrenal catecholamine content (57%). Our present findings suggest that tobacco SE to both dams and their pups during lactation causes malnutrition in early life that programs for obesity and hormonal and metabolic disturbances in adulthood, only if the pups are submitted to the same smoke environment as the mother.

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“…Bambace and cols. (27) demonstrated that the increase in diameter of the epicardial adipocyte is associated with a decreased EAT adiponectin expression in subjects with metabolic syndrome compared with subjects without it. Interestingly, intracoronary adiponectin levels reflect the systemic concentration of this hormone, and EAT contributes, in part, to such plasma levels (28).…”

Section: Discussionmentioning

confidence: 99%

Epicardial adipose tissue thickness and its association with adiponectin in metabolic syndrome patients from Mérida, Venezuela

Lima-Martínez

López-Mendez

Odreman

et al. 2014

Arq Bras Endocrinol Metab

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Objective: To study the relationship between epicardial adipose tissue (EAT) thickness and plasma levels of adiponectin in Venezuelan patients. Subjects and methods: Thirty-one patients diagnosed with metabolic syndrome (study group) and 27 controls were selected and tested for glycemia, lipids, and adiponectin. EAT thickness, ejection fraction, diastolic function, left ventricular mass (LVM), and left atrial volume (LAV) were determined by transthoracic echocardiography. Results: EAT thickness was greater in metabolic syndrome patients (5.69 ± 1.12 vs. RESUMOObjetivo: Estudar a relação entre a espessura do tecido adiposo epicárdico (TAE) e os níveis plasmáticos de adiponectina em pacientes venezuelanos. Sujeitos e métodos: Foram selecionados 31 pacientes com diagnóstico de síndrome metabólica (SM) (grupo de estudo) e 27 controles. Foram medidos a glicose, os lipídios e a adiponectina. Foram determinados a espessura do TAE, a fração de ejeção, a função diastólica, a massa ventricular esquerda (MVE) e o volume atrial esquerdo (VAI) pela ecocardiografia transtorácica. Resultados: A espessura do TAE foi maior em pacientes com SM (5,69 ± 1,12 contra 3,52 ± 0,80 mm; p = 0,0001) com uma correlação positiva com o índice de massa corporal (IMC) (r = 0,661; p = 0,0001), circunferência da cintura (CC) (r = 0,664; p = 0,0001), pressão arterial sistólica (PAS) (r = 0,607; p = 0,0001), diastólica (PAD) (r = 0,447; p = 0,0001), insulina (r = 0,505; p = 0,0001), com a relação TG/HDL-C (r = 0,447; p = 0,0001), com o colesterol HDL (r = 0,353; p = 0,007), VAI (r = 0,432; p = 0,001) e MVI (r = 0,469; p = 0,0001). A espessura do TAE se correlacionou negativamente com a adiponectina (r = -0,499; p = 0,0001). Conclusão: Existe uma relação significativa entre a espessura do TAE, os componentes do SM e a concentração plasmática de adiponectina, o que poderia ser utilizado como um biomarcador para essa doença. Arq Bras Endocrinol Metab. 2014;58(4):352-61 Descritores Tecido adiposo epicárdico; gordura epicárdica; síndrome metabólica; adiponectina; hispânicos

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Adiponectin gene expression and adipocyte diameter: a comparison between epicardial and subcutaneous adipose tissue in men

Cited by 102 publications

References 5 publications

Adipose morphology and metabolic disease

Adipose morphology and metabolic disease

Endocrine effects of tobacco smoke exposure during lactation in weaned and adult male offspring

Epicardial adipose tissue thickness and its association with adiponectin in metabolic syndrome patients from Mérida, Venezuela

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