&lt;p&gt;Reduced Beige Adipogenic Potential in Subcutaneous Adipocytes Derived from Obese Chinese Individuals&lt;/p&gt;

Li, Han; Shen, Lin; Zhang, Lei; Yan, Bing; Sun, Tao; Guo, Feng; Yin, Xiaolin

doi:10.2147/dmso.s248112

Cited by 8 publications

(5 citation statements)

References 26 publications

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“…Furthermore, adipocytes differentiated from subcutaneous abdominal WAT derived from obese individuals had lower UCP1 protein levels than that from lean persons [ 183 ]. Another report indicated that brown adipogenic potentials, such as thermogenic gene expression, oxygen consumption rate, and lipolysis ability, were impaired in preadipocytes isolated from subcutaneous fat tissues of obese individuals [ 184 ]. Although gender differences in the prevalence of BAT are still controversial, the thermogenic response to cold exposure was greater in females than in males, implying that sex steroids might contribute to different thermogenic processes [ 185 , 186 , 187 ].…”

Section: Obesity and Mitochondrial Metabolismmentioning

confidence: 99%

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Takeda

Harada

Yoshikawa

et al. 2023

IJMS

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Brown fats specialize in thermogenesis by increasing the utilization of circulating blood glucose and fatty acids. Emerging evidence suggests that brown adipose tissue (BAT) prevents the incidence of obesity-associated metabolic diseases and several types of cancers in humans. Mitochondrial energy metabolism in brown/beige adipocytes regulates both uncoupling protein 1 (UCP1)-dependent and -independent thermogenesis for cold adaptation and the utilization of excess nutrients and energy. Many studies on the quantification of human BAT indicate that mass and activity are inversely correlated with the body mass index (BMI) and visceral adiposity. Repression is caused by obesity-associated positive and negative factors that control adipocyte browning, de novo adipogenesis, mitochondrial energy metabolism, UCP1 expression and activity, and noradrenergic response. Systemic and local factors whose levels vary between lean and obese conditions include growth factors, inflammatory cytokines, neurotransmitters, and metal ions such as selenium and iron. Modulation of obesity-associated repression in human brown fats is a promising strategy to counteract obesity and related metabolic diseases through the activation of thermogenic capacity. In this review, we highlight recent advances in mitochondrial metabolism, thermogenic regulation of brown fats, and human metabolic diseases.

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Section: Obesity and Mitochondrial Metabolismmentioning

confidence: 99%

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Takeda

Harada

Yoshikawa

et al. 2023

IJMS

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“…Beige adipocytes lose UCP1 expression and mitochondrial density without persistent stimulation [ 71 ]. The expression of beige genes in subcutaneous fat is dysregulated in obese individuals [ 72 , 73 , 74 ]. In addition, there are methodological limitations in evaluating the activity of beige adipocytes in humans [ 56 ].…”

Section: Adipose Tissuementioning

confidence: 99%

Obesity and Endothelial Function

Kajikawa

Higashi

2022

Biomedicines

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Obesity is a major public health problem and is related to increasing rates of cardiovascular morbidity and mortality. Over 1.9 billion adults are overweight or obese worldwide and the prevalence of obesity is increasing. Obesity influences endothelial function through obesity-related complications such as hypertension, dyslipidemia, diabetes, metabolic syndrome, and obstructive sleep apnea syndrome. The excess fat accumulation in obesity causes adipocyte dysfunction and induces oxidative stress, insulin resistance, and inflammation leading to endothelial dysfunction. Several anthropometric indices and imaging modalities that are used to evaluate obesity have demonstrated an association between obesity and endothelial function. In the past few decades, there has been great focus on the mechanisms underlying endothelial dysfunction caused by obesity for the prevention and treatment of cardiovascular events. This review focuses on pathophysiological mechanisms of obesity-induced endothelial dysfunction and therapeutic targets of obesity.

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“…Most of the data regarding hBAT activity come from populations with obesity [ 9 , 10 , 14 ], which can not determine the causal relationship between inactive BAT and obesity (i.e., whether defective BAT contributes to obesity or vice-versa). Hence, the present study aimed to detect the browning capacity of subcutaneous WAT in overweight individuals and explore if the sympathetic-induced browning potential of subcutaneous WAT changes at a pre-obesity stage.…”

Section: Discussionmentioning

confidence: 99%

Compromised browning plasticity of primary subcutaneous adipocytes derived from overweight Chinese adults

Yao

Sun

et al. 2020

Diabetol Metab Syndr

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Purpose People with obesity have a compromised browning capacity of adipose tissue when faced with sympathetic stimuli. This study aimed to determine whether norepinephrine treatment can enhance the induction of precursor cells from human white adipose tissue to differentiate into adipocytes that express key markers of beige adipocytes, and if there is a difference in this capacity between normal weight and overweight individuals. Methods Stromal vascular cells derived from subcutaneous white adipose tissue of normal weight and overweight groups were induced to differentiation, with or without norepinephrine, into adipocytes. Oxygen consumption rate, lipolysis, the expression of uncoupling protein 1 and other thermogenic genes were compared between different adiposity and treatment groups. Results Peroxisome proliferator activated receptor γ- coactivator-1 alpha (PGC-1 α) and uncoupling protein 1 gene expression increased significantly in the normal weight group, but not in the overweight group, with norepinephrine treatment. The increments of lipolysis and oxygen consumption rate were also higher in adipocytes from the normal weight group with norepinephrine treatment, as compared with those of the overweight group. PR domain containing protein 16 (PRDM 16) gene expression was higher in the normal weight group compared with that in the overweight group, while there were no significant changes found with norepinephrine treatment in either the normal weight or overweight group. Conclusions Adipogenic precursor cells derived from overweight individuals were less prone to differentiate into beige-like adipocytes when facing sympathetic stimuli than normal weight ones, resulting in the compromised sympathetic-induced browning capacity in subcutaneous white adipose tissue in overweight individuals, which occurred before the onset of overt obesity.

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<p>Reduced Beige Adipogenic Potential in Subcutaneous Adipocytes Derived from Obese Chinese Individuals</p>

Cited by 8 publications

References 26 publications

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Mitochondrial Energy Metabolism in the Regulation of Thermogenic Brown Fats and Human Metabolic Diseases

Obesity and Endothelial Function

Compromised browning plasticity of primary subcutaneous adipocytes derived from overweight Chinese adults

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