We are analyzing https://link.springer.com/article/10.1007/s00018-022-04401-3.

Title:
Contribution of specific ceramides to obesity-associated metabolic diseases | Cellular and Molecular Life Sciences
Description:
Ceramides are a heterogeneous group of bioactive membrane sphingolipids that play specialized regulatory roles in cellular metabolism depending on their characteristic fatty acyl chain lengths and subcellular distribution. As obesity progresses, certain ceramide molecular species accumulate in metabolic tissues and cause cell-type-specific lipotoxic reactions that disrupt metabolic homeostasis and lead to the development of cardiometabolic diseases. Several mechanisms for ceramide action have been inferred from studies in vitro, but only recently have we begun to better understand the acyl chain length specificity of ceramide-mediated signaling in the context of physiology and disease in vivo. New discoveries show that specific ceramides affect various metabolic pathways and that global or tissue-specific reduction in selected ceramide pools in obese rodents is sufficient to improve metabolic health. Here, we review the tissue-specific regulation and functions of ceramides in obesity, thus highlighting the emerging concept of selectively inhibiting production or action of ceramides with specific acyl chain lengths as novel therapeutic strategies to ameliorate obesity-associated diseases.
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Keywords {🔍}

ceramide, pubmed, google, scholar, ceramides, cas, central, insulin, metabolic, obesity, mitochondrial, cell, cers, synthesis, fatty, lipid, effects, mice, resistance, species, muscle, specific, liver, increased, biol, obese, diabetes, cells, content, membrane, metabolism, hepatic, glucose, accumulation, levels, role, chain, inhibition, signaling, homeostasis, tissue, stress, chem, regulation, protein, metab, studies, disease, novo, function,

Topics {✒️}

jnk c-jun-n-terminal kinase long-chain-fatty-acid-coa ligase ceramide-initiated sapk/jnk signalling fa-coa fatty acyl-coenzyme methyl-branched long-chain bases tumor necrosis factor-alpha appetite-regulating agouti-related peptide high-fat diet-fed mice high-fat diet-dependent increase high-fat diet-fed rats c16-ceramide-induced channel formation form ultra-long-chain ceramides c26-coa-dependent ceramide synthesis high-fat diet-fed fixed acyl chain length branched long-chain bases rna-activated protein kinase high-fat diet feeding ceramide acyl-chain length diet-induced mitochondrial fragmentation sphingolipid n-acyl chain cell-type-specific lipotoxic reactions intestinal cers4-dependent ceramide synthesis cell-type-specific adverse reactions asah n-acylsphingosine aminohydrolase cgt ceramide udp-galactosyltransferase vesicle-bound intercellular transfer high-fat diet exposure sphingoid long-chain bases endoplasmic reticulum-mitochondria junction mediates lipid-induced inflammation methionine-choline deficient diet short-term mechanical unloading ceramide-activated protein kinase ceramide-dependent regulatory networks diet-induced insulin resistance chain length-specific properties fatty acid-induced lipotoxicity long-chain sphingolipid species protein-lipid overlay assays palmitate-induced mitochondrial fragmentation tumor necrosis factor ameliorates ceramide-induced lipotoxicity obesity-induced cers6-dependent c16 hypothalamic pgc-1alpha protects diet providing precursor substrates ormdl/orm-serine palmitoyltransferase membrane-emanating signaling cascades developing tissue-restrictive drugs mouse strain-dependent variation

Questions {❓}

Amati F et al (2011) Skeletal muscle triglycerides, diacylglycerols, and ceramides in insulin resistance: another paradox in endurance-trained athletes?
Bionda C et al (2004) Subcellular compartmentalization of ceramide metabolism: MAM (mitochondria-associated membrane) and/or mitochondria?
Is it possible to modulate ceramide metabolism for the treatment of obesity-related diseases?
Pewzner-Jung Y, Ben-Dor S, Futerman AH (2006) When do Lasses (longevity assurance genes) become CerS (ceramide synthases)?
Summers SA (2018) Could ceramides become the new cholesterol?

Schema {🗺️}

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         headline:Contribution of specific ceramides to obesity-associated metabolic diseases
         description:Ceramides are a heterogeneous group of bioactive membrane sphingolipids that play specialized regulatory roles in cellular metabolism depending on their characteristic fatty acyl chain lengths and subcellular distribution. As obesity progresses, certain ceramide molecular species accumulate in metabolic tissues and cause cell-type-specific lipotoxic reactions that disrupt metabolic homeostasis and lead to the development of cardiometabolic diseases. Several mechanisms for ceramide action have been inferred from studies in vitro, but only recently have we begun to better understand the acyl chain length specificity of ceramide-mediated signaling in the context of physiology and disease in vivo. New discoveries show that specific ceramides affect various metabolic pathways and that global or tissue-specific reduction in selected ceramide pools in obese rodents is sufficient to improve metabolic health. Here, we review the tissue-specific regulation and functions of ceramides in obesity, thus highlighting the emerging concept of selectively inhibiting production or action of ceramides with specific acyl chain lengths as novel therapeutic strategies to ameliorate obesity-associated diseases.
         datePublished:2022-07-05T00:00:00Z
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            Ceramide acyl chain length
            Sphingolipids
            Lipid signaling
            Lipotoxicity
            High-fat diet
            Obesity
            Insulin resistance
            Diabetes
            Metabolic disease treatment
            Cell Biology
            Biomedicine
            general
            Life Sciences
            Biochemistry
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      headline:Contribution of specific ceramides to obesity-associated metabolic diseases
      description:Ceramides are a heterogeneous group of bioactive membrane sphingolipids that play specialized regulatory roles in cellular metabolism depending on their characteristic fatty acyl chain lengths and subcellular distribution. As obesity progresses, certain ceramide molecular species accumulate in metabolic tissues and cause cell-type-specific lipotoxic reactions that disrupt metabolic homeostasis and lead to the development of cardiometabolic diseases. Several mechanisms for ceramide action have been inferred from studies in vitro, but only recently have we begun to better understand the acyl chain length specificity of ceramide-mediated signaling in the context of physiology and disease in vivo. New discoveries show that specific ceramides affect various metabolic pathways and that global or tissue-specific reduction in selected ceramide pools in obese rodents is sufficient to improve metabolic health. Here, we review the tissue-specific regulation and functions of ceramides in obesity, thus highlighting the emerging concept of selectively inhibiting production or action of ceramides with specific acyl chain lengths as novel therapeutic strategies to ameliorate obesity-associated diseases.
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      dateModified:2022-07-05T00:00:00Z
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         Atherosclerosis
         Ceramide acyl chain length
         Sphingolipids
         Lipid signaling
         Lipotoxicity
         High-fat diet
         Obesity
         Insulin resistance
         Diabetes
         Metabolic disease treatment
         Cell Biology
         Biomedicine
         general
         Life Sciences
         Biochemistry
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         name:Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany
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         name:Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
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               type:PostalAddress
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            address:
               name:Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany
               type:PostalAddress
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               name:Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
               type:PostalAddress
            type:Organization
      name:Jens C. Brüning
      affiliation:
            name:Max Planck Institute for Metabolism Research
            address:
               name:Department of Neuronal Control of Metabolism, Max Planck Institute for Metabolism Research, Cologne, Germany
               type:PostalAddress
            type:Organization
            name:University Hospital Cologne
            address:
               name:Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany
               type:PostalAddress
            type:Organization
            name:University of Cologne
            address:
               name:Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
               type:PostalAddress
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      name:Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Cologne, Germany
      name:Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany
      name:National Center for Diabetes Research (DZD), Neuherberg, Germany

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