Difference between revisions of "Koliaki 2015 Cell Metab"
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{{Publication | {{Publication | ||
|title=Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M (2015) Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab 21:739-46. | |title=Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M (2015) Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab 21:739-46. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25955209 PMID: 25955209] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/25955209 PMID: 25955209 Open Access] | ||
|authors=Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M | |authors=Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M | ||
|year=2015 | |year=2015 | ||
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{{Labeling | {{Labeling | ||
|area=Respiration, Patients | |area=Respiration, Patients | ||
|diseases=Diabetes, Obesity, Other | |||
|organism=Human | |organism=Human | ||
|tissues=Liver | |tissues=Liver | ||
|preparations=Homogenate, Isolated mitochondria | |preparations=Homogenate, Isolated mitochondria | ||
|topics=Substrate | |topics=Substrate | ||
|couplingstates=LEAK, OXPHOS, | |couplingstates=LEAK, OXPHOS, ET | ||
|pathways=F, N, NS, | |pathways=F, N, NS, Other combinations, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 10:44, 5 January 2018
| Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M (2015) Adaptation of hepatic mitochondrial function in humans with non-alcoholic fatty liver is lost in steatohepatitis. Cell Metab 21:739-46. |
Koliaki C, Szendroedi J, Kaul K, Jelenik T, Nowotny P, Jankowiak F, Herder C, Carstensen M, Krausch M, Knoefel WT, Schlensak M, Roden M (2015) Cell Metab
Abstract: The association of hepatic mitochondrial function with insulin resistance and non-alcoholic fatty liver (NAFL) or steatohepatitis (NASH) remains unclear. This study applied high-resolution respirometry to directly quantify mitochondrial respiration in liver biopsies of obese insulin-resistant humans without (n = 18) or with (n = 16) histologically proven NAFL or with NASH (n = 7) compared to lean individuals (n = 12). Despite similar mitochondrial content, obese humans with or without NAFL had 4.3- to 5.0-fold higher maximal respiration rates in isolated mitochondria than lean persons. NASH patients featured higher mitochondrial mass, but 31%-40% lower maximal respiration, which associated with greater hepatic insulin resistance, mitochondrial uncoupling, and leaking activity. In NASH, augmented hepatic oxidative stress (H2O2, lipid peroxides) and oxidative DNA damage (8-OH-deoxyguanosine) was paralleled by reduced anti-oxidant defense capacity and increased inflammatory response. These data suggest adaptation of the liver ("hepatic mitochondrial flexibility") at early stages of obesity-related insulin resistance, which is subsequently lost in NASH.
• O2k-Network Lab: DE Duesseldorf Roden M
Labels: MiParea: Respiration, Patients
Pathology: Diabetes, Obesity, Other
Organism: Human Tissue;cell: Liver Preparation: Homogenate, Isolated mitochondria
Regulation: Substrate Coupling state: LEAK, OXPHOS, ET Pathway: F, N, NS, Other combinations, ROX HRR: Oxygraph-2k
