We are analyzing https://link.springer.com/article/10.1007/s00125-016-3940-5.

Title:
Hepatic glucose and lipid metabolism | Diabetologia
Description:
The liver has a central role in the regulation of systemic glucose and lipid fluxes during feeding and fasting and also relies on these substrates for its own energy needs. These parallel requirements are met by coordinated control of carbohydrate and lipid fluxes into and out of the Krebs cycle, which is highly tuned to nutrient availability and heavily regulated by insulin and glucagon. During progression of type 2 diabetes, hepatic carbohydrate and lipid biosynthesis fluxes become elevated, thus contributing to hyperglycaemia and hypertriacylglycerolaemia. Over this interval there are also significant fluctuations in hepatic energy state. To date, it is not known to what extent abnormal glucose and lipid fluxes are causally linked to altered energy states. Recent evidence that the glucose-lowering effects of metformin appear to be mediated by attenuation of hepatic energy generation places an additional spotlight on the interdependence of hepatic biosynthetic and oxidative fluxes. The transition from fasting to feeding results in a significant re-direction of hepatic glucose and lipid fluxes and may also incur a temporary hepatic energy deficit. At present, it is not known to what extent these variables are additionally modified by type 2 diabetes and/or non-alcoholic fatty liver disease. Thus, there is a compelling need to measure fluxes through oxidative, gluconeogenic and lipogenic pathways and determine their relationship with hepatic energy state in both fasting and fed conditions. New magnetic resonance-based technologies allow these variables to be non-invasively studied in animal models and humans. This review summarises a presentation given at the symposium entitled ‘The liver in focus’ at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Kenneth Cusi, DOI: 10.1007/s00125-016-3952-1 , and by Hannele Yki-Järvinen, DOI: 10.1007/s00125-016-3944-1 ) and a commentary by the Session Chair, Michael Roden (DOI: 10.1007/s00125-016-3911-x ).
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Keywords {🔍}

hepatic, pubmed, google, scholar, cas, cycle, article, glucose, fluxes, energy, krebs, lipid, fatty, liver, metabolism, central, acid, conditions, metab, fasting, diabetes, state, gluconeogenesis, mitochondrial, oxidative, synthesis, physiol, type, endocrinol, jones, feeding, carbohydrate, insulin, disease, oxidation, nafld, rates, acetylcoa, lipogenesis, substrates, humans, nmr, plasma, nonalcoholic, metabolic, production, flux, information, generation, anaplerotic,

Topics {✒️}

magnetic resonance-based technologies vivo 13c-isotopomer high-fructose weight-maintaining diet gas chromatography-mass spectrometry de novo lipogenesis short-chain fatty acids gut-brain neural circuits branched-chain amino acids mild mitochondrial uncoupling 14c-labeled propionate metabolism mitochondrially generated acetyl-coa hyperinsulinaemic–hyperglycaemic clamp conditions fatty acid β-oxidation delgado tc cytosolic malonyl-coa levels including simple sugars krebs cycle metabolism stz-diabetes rat model krebs cycle flux adipose tissue lipolysis tca cycle flux hepatic krebs cycle fatty acid metabolism de-convoluting oxidative diet-induced nafld reflects hepatic lipogenesis promoting acetyl-coa generation article jones review summarises sunny ne citric acid cycle privacy choices/manage cookies krebs cycle fluxes krebs cycle driving 13c nmr study positional 13c-enrichment profiles perry rj hepatic energy metabolism attenuate pyruvate carboxylase 13c-enriched precursors hepatic intermediary metabolism 13c nmr measurements fatty liver disease [u-13c]propionate fatty acid synthesis lipogenic enzyme controlled mitochondrial energy generation [u-13c]glucose hepatic insulin resistance

Questions {❓}

A key question is: how are the changes in hepatic energy state related to those of hepatic glucose and lipid metabolic fluxes?
Given that, under fed conditions, glycolytic substrates appear to contribute at most ∼50% of the acetyl-CoA requirements for oxidation and that NEFA oxidation is efficiently repressed by malonyl-CoA, are there alternative substrates that could contribute to mitochondrial energy generation?

Schema {🗺️}

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         description:The liver has a central role in the regulation of systemic glucose and lipid fluxes during feeding and fasting and also relies on these substrates for its own energy needs. These parallel requirements are met by coordinated control of carbohydrate and lipid fluxes into and out of the Krebs cycle, which is highly tuned to nutrient availability and heavily regulated by insulin and glucagon. During progression of type 2 diabetes, hepatic carbohydrate and lipid biosynthesis fluxes become elevated, thus contributing to hyperglycaemia and hypertriacylglycerolaemia. Over this interval there are also significant fluctuations in hepatic energy state. To date, it is not known to what extent abnormal glucose and lipid fluxes are causally linked to altered energy states. Recent evidence that the glucose-lowering effects of metformin appear to be mediated by attenuation of hepatic energy generation places an additional spotlight on the interdependence of hepatic biosynthetic and oxidative fluxes. The transition from fasting to feeding results in a significant re-direction of hepatic glucose and lipid fluxes and may also incur a temporary hepatic energy deficit. At present, it is not known to what extent these variables are additionally modified by type 2 diabetes and/or non-alcoholic fatty liver disease. Thus, there is a compelling need to measure fluxes through oxidative, gluconeogenic and lipogenic pathways and determine their relationship with hepatic energy state in both fasting and fed conditions. New magnetic resonance-based technologies allow these variables to be non-invasively studied in animal models and humans. This review summarises a presentation given at the symposium entitled ‘The liver in focus’ at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Kenneth Cusi, DOI: 10.1007/s00125-016-3952-1 , and by Hannele Yki-Järvinen, DOI: 10.1007/s00125-016-3944-1 ) and a commentary by the Session Chair, Michael Roden (DOI: 10.1007/s00125-016-3911-x ).
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      headline:Hepatic glucose and lipid metabolism
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         De novo lipogenesis
         Deuterated water
          13C Isotopomer analysis
         Krebs cycle
         Magnetic resonance spectroscopy
         Pyruvate cycling
         Review
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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