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1 scle insulin resistance may be aggravated by intramyocellular accumulation of fatty acid-derived meta
3 er down-regulation, ceramide diminished both intramyocellular amino acid abundance and the phosphoryl
4 e children and adolescents with prediabetes, intramyocellular and intra-abdominal lipid accumulation
11 2 diabetes patients have higher unsaturated intramyocellular fat and blunted palmitate and linoleate
16 ffspring is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because
17 diabetes is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because
19 There were no differences between groups in intramyocellular glucose, as measured by biochemical ass
22 skeletal muscle as a predisposing factor for intramyocellular lipid (IMCL) accumulation and muscle in
25 Insulin resistance is closely related to intramyocellular lipid (IMCL) accumulation, and both are
26 scle fibers would exhibit similar changes in intramyocellular lipid (IMCL) and extramyocellular lipid
27 resistance correlates more tightly with the intramyocellular lipid (IMCL) concentration than with an
30 onal studies have shown correlations between intramyocellular lipid (IMCL) content and muscle strengt
36 he expression of BMPs, inflammation, HO, and intramyocellular lipid accumulation in both skeletal and
37 itivity, mitochondrial function, hepatic and intramyocellular lipid accumulation, cardiac energy stat
38 function, which predisposes IR offspring to intramyocellular lipid accumulation, which in turn activ
39 rate that burn injury results in a localized intramyocellular lipid accumulation, which in turn is ac
42 ectroscopy studies were performed to measure intramyocellular lipid and intrahepatic triglyceride con
44 s with impaired glucose tolerance had higher intramyocellular lipid content (3.04 [0.43] vs 1.99 [0.1
47 increased intrahepatic lipid content (IHL), intramyocellular lipid content (IMCL), and low circulati
48 me (P = .9), myocardial TG content (P = .9), intramyocellular lipid content (P = .3), or cardiac func
51 ed with an approximately 60% increase in the intramyocellular lipid content as assessed by H magnetic
53 iated with increases in hepatic (HTG) and/or intramyocellular lipid content, little is known about th
54 tion this is avoidable, given that causes of intramyocellular lipid deposition are predominantly life
57 scriptional oxidative phenotype, and altered intramyocellular lipid partitioning and may therefore be
59 conclude that insulin-resistant, maladapted intramyocellular lipid storage and turnover in patients
63 esonance imaging, and intrahepatic lipid and intramyocellular lipid were assessed by proton magnetic
64 magnetic resonance imaging and muscle lipid (intramyocellular lipid) by proton magnetic resonance spe
65 Recent studies have demonstrated increased intramyocellular lipid, decreased mitochondrial ATP synt
66 A levels of regulatory components related to intramyocellular lipid, glucose metabolism and fiber siz
67 ance have been linked to accumulation of the intramyocellular lipid-intermediate diacylglycerol (DAG)
68 taneous (SAT) adipose tissue, liver fat, and intramyocellular lipids (IMCL) in 101 Chinese, 82 Malays
69 one marrow fat content, of soleus muscle for intramyocellular lipids (IMCL), and liver for intrahepat
70 metabolism, resulting in increased levels of intramyocellular lipids (IMCLs) and lipid intermediates,
71 lin resistant, demonstrated higher levels of intramyocellular lipids (IMCLs), and expressed approxima
72 ent understanding of the effects of elevated intramyocellular lipids on insulin signaling and how the
73 ut exercise on skeletal muscle mitochondria, intramyocellular lipids, and insulin sensitivity index (
74 s between BMI and unsaturated fatty acids in intramyocellular lipids, and methylene groups in extramy
75 fetuin-A, body composition, pancreatic fat, intramyocellular lipids, fecal SCFAs, blood pressure, or
76 pecific skeletal muscle proteins involved in intramyocellular lipids, mitochondrial oxidative capacit
77 by a high oxidative capacity, have elevated intramyocellular lipids, yet are highly insulin sensitiv
78 ulin in adipocytes may be inhibited, whereas intramyocellular lipogenesis via the MAP kinase pathway
79 atty acids (NEFA) are trafficked directly to intramyocellular long-chain acylcarnitines (imLCAC) rath
81 P-MRS to measure changes in cytosolic [ADP] (intramyocellular marker of oxidative metabolism), oxidat
85 n of FIT2 (CKF2) had significantly increased intramyocellular triacylglyceride and complete protectio
87 reased energy metabolism and accumulate more intramyocellular triacylglycerol but have normal glucose
88 Mounting evidence indicates that elevated intramyocellular triacylglycerol concentrations are asso
97 tant muscle and that the association between intramyocellular triglycerides (IMTG) and insulin resist
98 ylcarnitines (imLCAC) rather than transiting intramyocellular triglycerides (imTG) on the way to rest
99 Chronic exercise and obesity both increase intramyocellular triglycerides (IMTGs) despite having op
101 ion, glycogen synthesis, and accumulation of intramyocellular triglycerides have all been linked with