Inter-tissue expression patterns of the key metabolic biomarker PGC-1α in severely obese individuals: Implication in obesity-induced disease

Balampanis, Konstantinos; Chasapi, Athina; Kourea, Eleni; Tanoglidi, Anna; Hatziagelaki, Erifili; Lambadiari, Vaia; Dimitriadis, George; Lambrou, George Ι.; Kalfarentzos, Fotios; Melachrinou, Maria; Sotiropoulou-Bonikou, Georgia

doi:10.1016/j.hjc.2018.08.002

Cited by 13 publications

(20 citation statements)

References 107 publications

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“…WAT browning could be enhanced through the induction of Ucp1 expression and/or mitochondrial oxidative metabolism (Mao et al 2018). Pgc1α, a browning-related gene, was known as a significant regulator of mitochondrial biogenesis, oxidative phosphorylation and fatty acid metabolism (Balampanis et al 2018). Both liraglutide and food restriction significantly upregulated the mRNA expression levels of Ucp1 in the inguinal and cluneal WAT, and the expression of Ucp1 was increased most by the high-dose of liraglutide (Fig.…”

Section: Figurementioning

confidence: 94%

The key role of a glucagon-like peptide-1 receptor agonist in body fat redistribution

Zhao

Zhu

Lü

et al. 2019

Journal of Endocrinology

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Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are an ideal therapy for type 2 diabetes and, as of recently, for obesity. In contrast to visceral fat, subcutaneous fat appears to be protective against metabolic diseases. Here, we aimed to explore whether liraglutide, a GLP-1RA, could redistribute body fat via regulating lipid metabolism in different fat depots. After being fed a high-fat diet for 8 weeks, 50 male Wistar and Goto-Kakizaki rats were randomly divided into a normal control group, a diabetic control group, low-and high-dose liraglutide-treated groups and a diet-control group. Different doses of liraglutide (400 μg/kg/day or 1200 μg/kg/day) or an equal volume of normal saline were administered to the rats subcutaneously once a day for 12 weeks. Body composition and body fat deposition were measured by dual-energy X-ray absorptiometry and MRI. Isotope tracers were infused to explore lipid metabolism in different fat depots. Quantitative real-time PCR and Western blot analyses were conducted to evaluate the expression of adipose-related genes. The results showed that liraglutide decreased visceral fat and relatively increased subcutaneous fat. Lipogenesis was reduced in visceral white adipose tissue (WAT) but was elevated in subcutaneous WAT. Lipolysis was also attenuated, and fatty acid oxidation was enhanced. The mRNA expression levels of adipose-related genes in different tissues displayed similar trends after liraglutide treatment. In addition, the expression of browning-related genes was upregulated in subcutaneous WAT. Taken together, the results suggested that liraglutide potentially redistributes body fat and promotes browning remodeling in subcutaneous WAT to improve metabolic disorders.

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Section: Figurementioning

confidence: 94%

The key role of a glucagon-like peptide-1 receptor agonist in body fat redistribution

Zhao

Zhu

Lü

et al. 2019

Journal of Endocrinology

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“…Moreover, the generation of ROS after treatment with visfatin was found to be dependent on de novo transcription and translation. "Taken together, these novel findings provide us with useful information regarding the key role of visfatin and NF-κB in skeletal muscle and therefore in the pathophysiological mechanism of insulin resistance" [10,11,23].…”

Section: Introductionmentioning

confidence: 87%

“…As we have mentioned previously, "all NF-κB family members are able to form homo-or heterodimers directing the dimer to a specific set of target genes. NF-κB is deemed the key modulator of inflammation because its activity level is increased and its mediated signalling is associated with a long list of inflammatory and pathological entities" [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

“…This phosphorylation promotes the degradation of IκBα, exposing the NLS of NF-κB and subsequently causing NF-κB to move to the nucleus where it induces the gene expression of inflammatory mediators. "Numerous NF-κB target genes, such as the tumour necrosis factor a (TNFα), interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1), are also involved in the development of obesity-induced insulin resistance" [10,11,14].…”

Section: Introductionmentioning

confidence: 99%

“…Our aim is to morphologically evaluate the effect of the inflammatory regulator NF-κB on ERβ and NFAT signalling pathways and the cross-talk with the co-regulator PGC1a in morbid obesity. We have already demonstrated that PGC1a plays an essential role in human metabolism [10,11] and there is plenty of data in the literature suggesting that the underlying inflammation in morbidly obese individuals is mediated via NF-κB signalling pathway. For our work, we applied the well-established method of immunohistochemistry in five different tissues of patients with morbid obesity who underwent planned bariatric surgery and we also performed an "in situ" assessment of the subcellular localization of the above mentioned biomarkers.…”

Section: Introductionmentioning

confidence: 99%

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NF-κB; the Critical Link between Immune and Metabolic Pathways: Could NF-κB be Used as a Novel Diagnostic and Prognostic Biomarker for Non-Alcoholic Steatohepatitis?

Chasapi¹,

Balampanis²,

Tanoglidi³

et al. 2019

obm hg

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Background: A great number of inflammatory mediators and metabolic biomarkers have been shown to contribute to the development and progression of obesity-induced pathologies, including insulin resistance and non-alcoholic fatty liver disease (NAFLD). Many of those mediators are either targets or activators of Nuclear Factor-κappa B (NF-κB), which is a key transcription factor that plays a pivotal role in the homeostasis and regulation of inflammatory signaling pathways in the liver. Methods: Our study population consists of 50 morbidly obese patients undergoing planned bariatric surgery, during which biopsies were taken from the visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), skeletal muscle (SM), extramyocellular adipose tissue (EMAT) and the liver. We evaluated the differential protein expression of NF-κB, ERβ (Estrogen Receptor β), NFATc1 (Nuclear factor of activated T-cells) and PGC1a (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) by immunohistochemistry. Results: We found that NF-κB is the key biomarker in a complicated intra-and inter-tissue co-expression network that interconnects metabolic and immune signaling pathways. We also demonstrated a possible role in lipid metabolism and the development of skeletal muscle insulin resistance and non-alcoholic steatohepatitis (NASH). Conclusions: Our findings suggest that NF-κB may be the critical link between immune and metabolic pathways and could represent a future preventive and therapeutic target against obesity-induced metabolic diseases. We hope that our study will contribute to the better understanding of the complex inter-tissue connections that are disrupted in obesity and its associated comorbidities.

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Intramuscular mitochondrial and lipid metabolic changes of rats after regular high-intensity interval training (HIIT) of different training periods

Shangguan

Luo

et al. 2023

Mol Biol Rep

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Background: High-intensity Interval Training (HIIT) is a time-efficient form of exercise and has gained popularity in recent years. However, at molecular level, the understanding about the effects of HIIT is not comprehensive, and even less is elucidated about HIIT of different training duration cycles, although different durations always lead to different post-training consequences. Method: In this study, by training SD rats using HIIT protocols lasting for different training duration cycles, we investigated the adaptive response of intramuscular triglyceride abundance and mitochondria enhancement after HIIT training (2, 4, 6, 8, and 10 weeks). We selected 72h after the last session of training as the time point of sacrifice. Results:The suppressed activation of the cAMP-PKA pathway indicates that skeletal muscle was in the recovery phase at this time point. Intramuscular triglyceride abundance was significantly elevated after 2, 4, and 10 weeks of HIIT. However, the lipid metabolism-related proteins inconsistently changed in a chaotic trend (see Table . 1). The expression levels of PGC1-α and COX IV decreased after 2 and 4 weeks of training and began to rise when the training duration reached 6 weeks. Interestingly, the variation tendency of PGC1-α and COX IV is very similar to that of CPT-1B. Conclusion:Given the fact that CPT-1B is responsible for the transfer of free fatty acids into the mitochondria to facilitate muscular lipid oxidation, there is a great possibility that: A) the IMTG accumulation observed within 0-4 weeks [defined as phase 1 here] of HIIT might be primarily attributed to damaged mitochondria oxidation capacity. B) when the training duration reached 6 weeks [defined as phase 2], mitochondria function and biogenesis began to be improved by training stimulus and might result in the disappearance of IMTG increase. We believe the phase 2 is rather similar to the condition of athletes`paradox, which should be a healthy adaptation induced by exercise training. Also, for HIIT Rat Modelling, intervention duration cycles longer than 4 weeks are recommended if similar HIIT frame of this study is used.

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Inter-tissue expression patterns of the key metabolic biomarker PGC-1α in severely obese individuals: Implication in obesity-induced disease

Cited by 13 publications

References 107 publications

The key role of a glucagon-like peptide-1 receptor agonist in body fat redistribution

The key role of a glucagon-like peptide-1 receptor agonist in body fat redistribution

NF-κB; the Critical Link between Immune and Metabolic Pathways: Could NF-κB be Used as a Novel Diagnostic and Prognostic Biomarker for Non-Alcoholic Steatohepatitis?

Intramuscular mitochondrial and lipid metabolic changes of rats after regular high-intensity interval training (HIIT) of different training periods

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