Læknablaðið : fylgirit - 01.09.1993, Blaðsíða 35

LÆKNAB LAÐIÐ/FYLGIRIT 24
33
Does a Long-term Primary Rat Hepatocyte Cult-
ure Suffer from a Carnitine Depletion.
‘b.G. B.jÖrnsson, G.F. Gibbons. Metabolic Re-
search Laboratory, Radcliffe Infirmary,
Oxford, U.K.
Hepatocytes from male Wistar rats were
isolated by a two-steps collagenase perfusion
technique of Seglen [1], and cultured for 24
h to 72 h in a Waymouth’s (MB 752/1) medium
supplemented with amino acids, pyruvate, lact-
ate, dexamethasone and oleate. In experi-
ments that lasted more than 24 h, culture
medium was changed every 24 h. At the end of
the final 24 h culture period, medium and
cells were collected, the VLDL fraction isol-
ated by centrifugation, and triacylglycerol
and cholesterol measured; cAMP was measured
by RIA; ketone bodies (acetoacetate, 5-hydr-
oxybutyrate) were assayed in the infranatant.
Over the 3-days culture period there was
little or no change in the rate of ketogenes-
is, however, a rather steep fall in ketogen-
esis was observed in the presence of glucagon
(10"7 M). Addition of carnitine (final conc.
0.5 mM) on the final day of culture enhanced
ketogenesis, but suppressed both cellular
triacylglycerol conc. and VLDL output (total
mass and [3H]-oleate incorporation). On the
first day of culture addition of carnitine
had no effect on the secretion of VLDL tri-
acylglycerol. Although on day 3 the cells re-
tained their ability to increase cAMP in re-
sponse to glucagon, their ketogenic response
to this hormone was reduced compared to that
on day 1 of culture. This decreased response
was also observed in the presence of carnitine
and suggests that cAMP was less able to stim-
ulate fatty acid oxidation after 3 days in
culture. Nevertheless, VLDL secretion remained
responsive to the inhibitory effect of for-
skolin under these circumstances which sug-
gests an uncoupling of the cAMP-mediated re-
gulation of hepatic lipid oxidation and lipid
secretion.- [1] Seglen, P.O. Methods Cell
Biol. 13:29 - 83, 1976.
V 5
Blóörauði, blóöfitur og hormón og
tengsl þeirra hjá körlum, 70 til 85
ára.
Matthías Kjeld, Gu&mundur Sigþórs-
son, Nikulós Sigfússon.
Rannsóknastofa Landspítalans, Rannsókna-
stofan í Domus Medica, Hjartavernd.
Eftir miójan aldur laekkar blóörauöi (Hb) í
körlum en hækkar lítillega eöa stendur í staö
í konum. Líkur eru til aö breytingar þessar
séu tengdar kynhormónum en karlhormón
örva haemopoiesis meöan kvenhormón
viröast hemja hana. Styrkur testosteróns í
sermi lækkar meö aldri, bæöi sá hlutinn sem
er próteinbundinn og hinn sem er frír [1]. Þá
hefur fundist jákvæö fylgni milli sermis HDL-
kólesteróls og sermis testósteróns styrks hjá
30 - 45 ára körlum [2]. Minna er vitaö um
tengsl þessara efna í eldri körlum. Viö höfum
því mælt Hb, frítt testósterón (FT), luteinizing
hormón (LH), kólesteról og HDL-kólesteról í
blóöi og sermi 400 - 500 heilbrigöra fastandi
karla á aldrinum 70 til 85 ára.
Gagnstætt því sem fundist hefur í
aldursdreiföari úrtökum lækkaöi kólesteról
meö aldri í þessum hópi (p<0.01). Einnig
lækkuöu Hb (p<0.02) og FT (0.001) en LH
hækkaöi (p~0.05) meö aldri. FT haföi
jákvæöa (p<0.02) og LH neikvæða (p<0.001)
fylgni viö Hb en hvorki viö kólesteról né HDL-
kólesterólstyrk. Niöur-stööur benda til aö
annaö samband sé á milli kynhormóna og
fituþátta í öldruöu fólki en í þvi yngra og
jafnframt aö kynhormón kunni aö tengjast
lækkun Hb styrks í blóöi fólks sem gerir vart
viö sig eftir miöjan aldur. Frekari könnun á
þessum þáttum meö fyllri upplýsingum um
lífsvenjur þessa fólks og líkamsbyggingu, t.d.
reykingar og Quetelet index, er fyrirhuguö.
Heimildir: 1) Simon D et al. Am J. Epidem
1992. 2) Freedman DS. Arterioscler Thromb
1991; 11: 307-14.