Increased serum concentration of ceramides in obese children with nonalcoholic fatty liver disease

Wasilewska, Natalia; Bobrus-Chociej, Anna; Harasim-Symbor, Ewa; Tarasów, Eugeniusz; Wojtkowska, Małgorzata; Chabowski, Adrian; Lebensztejn, Dariusz Marek

doi:10.1186/s12944-018-0855-9

Cited by 42 publications

(41 citation statements)

References 33 publications

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“…Additional analysis shows that sphingolipid species correlated with hepatic oxidative stress and inflammation (25). In a prospective study consisting of 31 children diagnosed with non-alcoholic fatty liver disease (NAFLD), Wasilewska et al demonstrated significant, positive correlation between total serum concentration of ceramides with insulin and also with HOMA-IR (26). Additionally, this study reveals that total ceramide concentration and specific (saturated fatty acyl) subspecies of ceramides such as C14, C16, C16:1, C18, and C18:1 were significantly higher in children with NAFLD compared to controls (26).…”

Section: Liver Diseasementioning

confidence: 99%

“…In a prospective study consisting of 31 children diagnosed with non-alcoholic fatty liver disease (NAFLD), Wasilewska et al demonstrated significant, positive correlation between total serum concentration of ceramides with insulin and also with HOMA-IR (26). Additionally, this study reveals that total ceramide concentration and specific (saturated fatty acyl) subspecies of ceramides such as C14, C16, C16:1, C18, and C18:1 were significantly higher in children with NAFLD compared to controls (26). Lastly, a randomized clinical trial conducted to determine the influence of dietary saturated and polyunsaturated fat on fatty liver development found that saturated fat markedly induces liver fat and serum ceramides (27).…”

Section: Liver Diseasementioning

confidence: 99%

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Ceramide Synthases Are Attractive Drug Targets for Treating Metabolic Diseases

Raichur

2020

Front. Endocrinol.

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Ceramide synthases (CerS) are central enzymes required for the de-novo synthesis of ceramides and other sphingolipids. They catalyze the addition of different acyl-chains to a sphingoid base, and thus account for much of the rich diversity in the sphingolipid family. Recent studies have demonstrated that the acyl-chain is an important determinant of ceramide function, such that a small subset of ceramides (e.g., those containing the C16 or C18 acyl-chain) alter metabolism by inhibiting insulin signaling or inducing mitochondrial fragmentation. Herein I discuss the therapeutic potential of targeting certain ceramide synthase isoforms for the treatment of obesity, insulin resistance, steatohepatitis, and other metabolic disorders.

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Section: Liver Diseasementioning

confidence: 99%

Section: Liver Diseasementioning

confidence: 99%

Ceramide Synthases Are Attractive Drug Targets for Treating Metabolic Diseases

Raichur

2020

Front. Endocrinol.

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“…Insulin resistance in skeletal muscle plays a key role in Type 2 diabetes development. Various studies support the importance of specific muscle ceramides in the development of lipid-induced skeletal muscle insulin resistance [61,62]; however, the role of ceramides as mediators of hepatic insulin resistance is unclear and supported by a few [7,63,64], but not all [65] studies, as recently reviewed [66]. The degradation of ceramides both in the liver and in fat tissue improved glucose metabolism, suggesting a major contributing role for both these tissues in regulating circulating ceramide levels, and, in addition, confirming the role of these substances on glucose homeostasis [7].…”

Section: Ceramides and Glucose Metabolismmentioning

confidence: 99%

Ceramides and diabetes mellitus: an update on the potential molecular relationships

Yaribeygi

Ruscica

et al. 2019

Diabet. Med.

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Recent evidence suggests that ceramides can play an important pathophysiological role in the development of diabetes. Ceramides are primarily recognized as lipid bilayer building blocks, but recent work has shown that these endogenous molecules are important intracellular signalling mediators and may exert some diabetogenic effects via molecular pathways involved in insulin resistance, β‐cell apoptosis and inflammation. In the present review, we consider the available evidence on the possible roles of ceramides in diabetes mellitus and introduce eight different molecular mechanisms mediating the diabetogenic action of ceramides, categorized into those predominantly related to insulin resistance vs those mainly implicated in β‐cell dysfunction. Specifically, the mechanistic evidence involves β‐cell apoptosis, pancreatic inflammation, mitochondrial stress, endoplasmic reticulum stress, adipokine release, insulin receptor substrate 1 phosphorylation, oxidative stress and insulin synthesis. Collectively, the evidence suggests that therapeutic agents aimed at reducing ceramide synthesis and lowering circulating levels may be beneficial in the prevention and/or treatment of diabetes and its related complications.

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“…Elevated levels of circulating free fatty acids (FFAs) combined with insulin resistance (IR) and excessive accumulation of triglycerides in liver cells serve a major role in the development of NAFLD (7). Additionally, lipid accumulation also responsible for oxidative stress, inflammatory response and lipotoxicity, predisposing patients to progressive liver injury (8). IR, lipotoxicity, inflammatory response, genetic polymorphisms, adipokines and intestinal flora can affect the pathogenesis of NAFLD (8).…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, lipid accumulation also responsible for oxidative stress, inflammatory response and lipotoxicity, predisposing patients to progressive liver injury (8). IR, lipotoxicity, inflammatory response, genetic polymorphisms, adipokines and intestinal flora can affect the pathogenesis of NAFLD (8). However, the interaction between these mechanisms and their changes in the occurrence and development of NAFLD remain to be determined.…”

Section: Introductionmentioning

confidence: 99%

Abnormal metabolic processes involved in the pathogenesis of non‑alcoholic fatty liver disease (Review)

Shao

Qin

et al. 2020

Exp Ther Med

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and can lead to liver cirrhosis or liver cancer in severe cases. In recent years, the incidence of NAFLD has increased substantially. The trend has continued to increase and has become a key point of concern for health systems. NAFLD is often associated with metabolic abnormalities caused by increased visceral obesity, including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, atherosclerosis and systemic microinflammation. Therefore, the pathophysiological mechanisms of NAFLD must be clarified to develop new drug treatment strategies. Recently, researchers have conducted numerous studies on the pathogenesis of NAFLD and have identified various important regulatory factors and potential molecular mechanisms, providing new targets and a theoretical basis for the treatment of NAFLD. However, the pathogenesis of NAFLD is extremely complex and involves the interrelationship and influence of multiple organs and systems. Therefore, the condition must be explored further. In the present review, the abnormal metabolic process, including glucose, lipid, amino acid, bile acid and iron metabolism are reviewed. It was concluded that NAFLD is associated with an imbalanced metabolic network that involves glucose, lipids, amino acids, bile acids and iron, and lipid metabolism is the core metabolic process. The current study aimed to provide evidence and hypotheses for research and clinical treatment of NAFLD.

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Increased serum concentration of ceramides in obese children with nonalcoholic fatty liver disease

Cited by 42 publications

References 33 publications

Ceramide Synthases Are Attractive Drug Targets for Treating Metabolic Diseases

Ceramide Synthases Are Attractive Drug Targets for Treating Metabolic Diseases

Ceramides and diabetes mellitus: an update on the potential molecular relationships

Abnormal metabolic processes involved in the pathogenesis of non‑alcoholic fatty liver disease (Review)

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