Steatosis in metabolic diseases: A focus on lipolysis and lipophagy

Zhao, Xingtao; Amevor, Felix Kwame; Cui, Zhifu; Wan, Yan; Xue, Xinyan; Peng, Cheng; Li, Yunxia

doi:10.1016/j.biopha.2023.114311

Cited by 10 publications

(6 citation statements)

References 169 publications

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“…Fatty acid is the principal form in which energy is stored in complex organisms and animals. The β‐oxidation of fatty acids is a key process in the catabolism of lipids in mammals (Houten et al, 2016; Zhao et al, 2023), which is also key to maintaining energy homeostasis (Adeva‐Andany et al, 2019). The study by Ardakanian et al (2022) also confirmed that olanzapine can lead to lipid metabolism disorders by inducing oxidative stress and increasing food intake and body weight.…”

Section: Discussionmentioning

confidence: 99%

Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

Zhu,

Zhao,

Chao

et al. 2024

Biomedical Chromatography

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As one of the most common antipsychotics, olanzapine may cause metabolic‐related adverse effects, but it is still unknown how olanzapine alters lipid metabolism. In this study, we found that olanzapine‐treated mice showed varying degrees of dyslipidemia, which was particularly pronounced in female mice. Based on ultra‐performance liquid chromatography–quadrupole time‐of‐flight–MS (UPLC–Q‐TOF–MS) technology and lipid metabolomics, we mapped the changes in lipid metabolism in olanzapine‐treated mice and then compared the changes in lipid metabolism between male and female mice. There were 98 metabolic differentiators between the olanzapine‐treated and control groups in females and 79 in males. These metabolites were glycerolipids, glycerophospholipids, fatty amides, and sphingolipids, which are involved in glycerolipid metabolism, glycerophospholipid metabolism, and fatty acid metabolism. These results suggest that olanzapine‐induced changes in the levels of lipid metabolites are closely associated with disturbances in lipid metabolic pathways, which may underlie lipemia. This lipidome profiling study not only visualizes changes in lipid metabolism in liver tissue but also provides a foundation for understanding the regulatory pathways and mechanisms involved in olanzapine‐induced lipid metabolism disorders. Furthermore, this study demonstrates differences in lipid metabolism between males and females, providing a reference for clinical treatment regimen selection.

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Section: Discussionmentioning

confidence: 99%

Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

Zhu,

Zhao,

Chao

et al. 2024

Biomedical Chromatography

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“…Regarding PPARα, it is a well-known transcription factor belonging to the nuclear receptor superfamily and is expressed in the liver, skeletal muscle, heart, adipose tissue, kidney, and other tissues, and it plays crucial roles in fatty acid catabolism, glucose metabolism, and the regulation of energy consumption and inflammation [ 19 ]. ATGL regulates SAT lipolysis by controlling the activity of PPARα in hepatocytes [ 20 ]. Importantly, during cachexia a concomitant inhibition of adipogenesis takes place, possibly triggered by PPAR α [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

“…ATGL regulates SAT lipolysis by controlling the activity of PPARα in hepatocytes [ 20 ]. Importantly, during cachexia a concomitant inhibition of adipogenesis takes place, possibly triggered by PPAR α [ 20 ]. In this light, our data may support this hypothesis, although we were not able to observe robust differences likely due to the small number of patients included in this analysis.…”

Section: Discussionmentioning

confidence: 99%

Assessment of lipolysis biomarkers in adipose tissue of patients with gastrointestinal cancer

Tambaro,

Imbimbo,

Ferraro

et al. 2024

Cancer Metab

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Background Adipose tissue metabolism may be impaired in patients with cancer. In particular, increased lipolysis was described in cancer-promoting adipose tissue atrophy. For this reason, we assessed the expression of the lipolysis-associated genes and proteins in subcutaneous adipose tissue (SAT) of gastrointestinal (GI) cancer patients compared to controls to verify their involvement in cancer, among different types of GI cancers, and in cachexia. Methods We considered patients with GI cancer (gastric, pancreatic, and colorectal) at their first diagnosis, with/without cachexia, and controls with benign diseases. We collected SAT and total RNA was extracted and ATGL, HSL, PPARα, and MCP1 were analyzed by qRT-PCR. Western blot was performed to evaluate CGI-58, PLIN1 and PLIN5. Results We found higher expression of ATGL and HSL in GI cancer patients with respect to controls (p ≤ 0.008) and a trend of increase for PPARα (p = 0.055). We found an upregulation of ATGL in GI cancer patients with cachexia (p = 0.033) and without cachexia (p = 0.017) vs controls. HSL was higher in patients with cachexia (p = 0.020) and without cachexia (p = 0.021), compared to controls. ATGL was upregulated in gastric cancer vs controls (p = 0.014) and higher HSL was found in gastric (p = 0.008) and in pancreatic cancer (p = 0.033) vs controls. At the protein level, we found higher CGI-58 in cancer vs controls (p = 0.019) and in cachectic vs controls (p = 0.029), as well as in gastric cancer vs controls (p = 0.027). Conclusion In our cohort of GI cancer patients, we found a modulation in the expression of genes and proteins involved in lipolysis, and differences were interestingly detected according to cancer type.

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“…As non-selective autophagy mechanisms have been completely explored, selective autophagy has gradually emerged as a hot spot for research in recent years [ 101 ]. Selective autophagy can be divided into different categories such as mitophagy [ 102 ], nuclear autophagy [ 103 ], endoplasmic reticulum autophagy [ 104 ] and lipophagy [ 105 ] depending on the target of its action. In contrast, mitochondria, as cellular energy hubs in eukaryotic cells, are susceptible to the damage caused by high levels of ROS thus leading to dysfunction and disruption of homeostasis [ 102 ].…”

Section: Mitophagy’s "Unique Role" In Cscs: Preservation Of Stemness ...mentioning

confidence: 99%

Crosstalk between autophagy and CSCs: molecular mechanisms and translational implications

Dai

Peng

et al. 2023

Cell Death Dis

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Cancer stem cells(CSCs) play a key role in regulating tumorigenesis, progression, as well as recurrence, and possess typical metabolic characteristics. Autophagy is a catabolic process that can aid cells to survive under stressful conditions such as nutrient deficiency and hypoxia. Although the role of autophagy in cancer cells has been extensively studied, CSCs possess unique stemness, and their potential relationship with autophagy has not been fully analyzed. This study summarizes the possible role of autophagy in the renewal, proliferation, differentiation, survival, metastasis, invasion, and treatment resistance of CSCs. It has been found that autophagy can contribute to the maintenance of CSC stemness, facilitate the tumor cells adapt to changes in the microenvironment, and promote tumor survival, whereas in some other cases autophagy acts as an important process involved in the deprivation of CSC stemness thus leading to tumor death. Mitophagy, which has emerged as another popular research area in recent years, has a great scope when explored together with stem cells. In this study, we have aimed to elaborate on the mechanism of action of autophagy in regulating the functions of CSCs to provide deeper insights for future cancer treatment.

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Steatosis in metabolic diseases: A focus on lipolysis and lipophagy

Cited by 10 publications

References 169 publications

Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

Olanzapine‐induced weight gain and lipid dysfunction in mice between different gender

Assessment of lipolysis biomarkers in adipose tissue of patients with gastrointestinal cancer

Crosstalk between autophagy and CSCs: molecular mechanisms and translational implications

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