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SUMMARY:INVOLVEMENT OF ECTOPIC FAT AND MITOCHONDRIAL FUNCTION IN TYPE 2 DI
 ABETES 
DTSTART:20101108T121500
DTSTAMP:20260405T204805Z
UID:3cf250d3567754be929f773fd9d8a4e1bec3c328b39364b4089bab74
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr Patrick Schrauwen\, Dept. of Human Biology\, Maastricht Uni
 versity Medical Center\, Maastricht\, The Netherlands\nObesity is the majo
 r risk factor for the development of type 2 diabetes mellitus. In obesity\
 , fat not only stores in white adipose tissue\, but fatty acids can also a
 ccumulate in ectopic fat stores like heart\, liver and muscle. Fat accumul
 ation in skeletal muscle is strongly associated with the development of sk
 eletal muscle insulin resistance\, and the latter is a first hallmark in t
 he development of type 2 diabetes mellitus. In the recent 5-6 years\, a re
 duced mitochondrial function in skeletal muscle has been proposed to under
 lie the accumulation of fat in skeletal muscle. In fact\, non-invasive in 
 vivo magnetic resonance spectroscopy has revealed a reduced mitochondrial 
 function combined with elevated muscular lipid content in type 2 diabetic 
 patients and in pre-diabetic first-degree relatives. Ex vivo measurements 
 have pointed towards reduced intrinsic mitochondrial function\, reductions
  in mitochondrial density and alterations in mitochondrial structure. It i
 s indeed tempting to suggest that these mitochondrial abnormalities could 
 be responsible for the accumulation of fat in muscle and thereby be linked
  to the development of insulin resistance. Alternatively\, however\, mitoc
 hondrial dysfunction may be the consequence of insulin resistance and/or m
 uscular fat accumulation. Thus\, the acute elevation of circulating fatty 
 acids reduces the expression of the transcriptional co-activator PGC1\, an
  important transcription factor in mitochondrial biogenesis. Furthermore\,
  fatty acids that accumulate in skeletal muscle cells may exert deleteriou
 s effects to mitochondrial function (lipotoxicity) via the formation of RO
 S-induced lipid peroxides. Indeed\, increased lipid peroxidation has been 
 reported in insulin resistant skeletal muscle. In addition\, studies perfo
 rmed in animals fed high-fat diets tend to indicate that muscular fat accu
 mulation precedes the development of mitochondrial dysfunction. In this pr
 esentation the current evidence for the role of mitochondrial dysfunction 
 in the etiology of muscular insulin resistance will be discussed. Furtherm
 ore\, it will be discussed if endurance training can reverse mitochondrial
  dysfunction.
LOCATION:SV1717a
STATUS:CONFIRMED
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