Læknablaðið - 15.12.1984, Síða 41

LÆKNABLADID
349
FEEDING AND STARVATION OF DONOR
ANIMAL CAUSE RESISTANCE TO THE
EFFECTS OF INSULIN AND GLUCAGON ON
LIPOGENESIS, RESPECTIVELY, IN ISOLATED
RAT HEPATOCYTES IN VITRO.
Ó. G. Bjömsson, C. R. Pullinger, and G. F.
Gibbons. MRC Lipid Metabolism Unit,
Hammersmith Hospital, London, U.K.
We have observed that although basal rates of lipo-
genesis (incubations in buffer alone) were higher in
hepatocytes prepared from ratr which had received
food for 6 h (188.8±9.8, SEM, n = 10, nmol 3H20
incorporated/mg protein) than from hepatocytes of
starved animals (82.9 ±18.4, P<0.05), insulin stimu-
lated lipogenesis to a greater extent in »starved«
hepatocytes (to 230 % of control) than in »fed«
hepatocytes (to 148 % of control). Also, whilst 102
pU/ml of insulin produced a significant increase (to
137 °/o, P<0.05) in cells prepared from starved rats
(16 h starvation), there was no significant change in
lipogenesis at that conc. of insulin in hepatocytes
from fed rats (to 103% of control). Long term
starvation (43 H) Iead, however, to complete lack of
fatty acid synthesis with or without insulin. We have
also observed that after prolonged starvation of
donor rats, the inhibiting effect on fatty acid
synthesis of incubation rat hepatocytes with gluca-
gon became relatively less obvious (83 % inhibition
in hepatocytes from fed rats, 60 % inhibition in
hepatocytes from rats starved for 19 h, and only
42 % inhibition in hepatocytes from rats starved for
43 h). We suggest that the relative resistance to
insulin stimulation in vitro in hepatocytes from fed
rats is due to occupation and downregulation of
insulin receptors in vivo during the 6 h feeding prior
to the experiments, when plasma levels of insulin
are high. There are therefore fewer insulin recep-
tors available for insulin binding in vitro which leads
to less effect during incubation. The lack of synthe-
sis during incubation with insulin in hepatocytes
from rats starved for 43 h was probably due to lack
of substrate, as the situation was partially reversed
by adding pyruvate to the incubation medium.
Similarly, we explain the relatively increased resi-
stance to glucagon inhibition of fatty acid synthesis
during increased starvation, as due to down-regula-
tion of the glucagon receptor, as plasma levels of
glucagon increase during starvation.
PHAGOCYTOSIS AND KILLING OF COMMON
BACTERIAL PATHOGENS OF THE LUNG BY
ALVEOLAR MACROPHAGES IN VITRO.
Steinn Jónsson, Daniel M. Musher, Alan
Chapman, Allen Goree & E. Clinton Lawrence.
To investigate the factors that determine susceptibi-
lity of the lungs to infection with common respirato-
ry pathogens, we studied phagocytosis and killing of
nontypable Haemophilus influenzae (NTHI), H.
influenzae type b (HITB), Streptococcus pneumoni-
ae (SP) types III, VI and XIV, an unencapsulated
variant of SP type III (SP III UN), and Staphyiococ-
cus aureus Cowan I (SA), using human alveotar
macrophages (AM) obtained by bronchoalveolar
lavage of healthy non-smokers. Radiolabeled bacte-
ria, opsonized in varying concentrations of pooled
normal human serum (PHS), were incubated with
AM in a ratio of 20:1. Phagecytosis was measured
by counting cell-associated with AM in a ratio of 20:
1. Phagocytosis was measured by counting cell-
associated radioactivity and is reported as percenta-
ge of total radioactivity present during incubation.
Uptake of bacteria was verified by electron micro-
scopy. Intracellular killing was determined by diluti-
on and inoculation of blood or chocolate agar plates
using appropriate controls. After opsonization with
10% PHS and incubation with AM for 20 minutes
the mean uptake (±standard deviation) of NTHI
(67.5 ± 15.9 %), SP type III UN (71.2 ±4.8 %) and SA
(79.1 ±10.2%) was significantly greater (p<0.01)
than that of HITB (40.1 + 15.0 %), and SP types III
(4.4+ 3.1 %), VI (11.8 + 9.6%) or XIV (8.7±7.0%).
NTHI was ingested well after opsonization with as
little as 2 % PHS, whereas the same degree of
uptake was never achieved for HITB despite
opsonization with up to 40 % PHS. Phagocytosis of
encapsulated SP was not significantly increased by
the addition of as much as 80 % PHS. Intracellular
killing of SP III UN and NTHI closely corresponded
to the degree of phagocytosis. Uptake of HITB and
the encapsulated SP were insufficient for accurate
assessment of killing. Despite a high degree of
uptake of SA, no intracellular killing was demon-
strated. We conclude that the virulence of S.
pneumoniae and H. Influenzae as lung pathogen is
determined jointly by encapsulation and the inad-
equate opsonizing effect of normal human serum,
whereas that of S. aureus may be related to
resistance to intracellular killing by AM.
Froin the Medical Service (Infectious Diseases and
Pulmonary Sections), Veterans Administration Medical
Center, Houston, Texas 77211, and the Departments of
Medicine, Microbiology and Immunology, Baylor Colle-
ge of Medicine, Houston, Texas 77030.
NATRÍUM í RAUÐUM BLÓÐKORNUM,
ÆTTARSAGA UM HÁÞRÝSTING OG AUKIN
SALTNEYSLA
Óttar Guömundsson. Lyflækningadeild og
Háþrýstideild Sahlgrenska sjúkrahússins,
Gautaborg.
Fyrir um 20 árum uppgötvuðu Losse og samstars-
menn, að natríummagn rauðra blóðfrumna var
aukið hjá sjúklingum með háprýsting og sumum
afkomendum þeirra. Þetta hefur síðar verið staðfest
af öðrum rannsóknarhópum og sýnt fram á, að pessi
aukning natríums í frumum sé vegna röskunar á
útdælingu natríums frá frumunum. Reynt hefur verið
að skýra próun háprýstings í Ijósi þessa. Peirri
tilgátu hefur verið varpað fram, að einstaklingar