Electronic Library of Scientific Literature - © Academic Electronic Press
Volume 36 / No. 4 / 2002
P. Simoncíkova, S. Wein, D. Gasperikova, J. Ukropec, M. Certik, I. Klimes, E. Sebokova
Diabetes and Nutrition Research Laboratory, Institute of Experimental Endocrinology, Slovak Academy of Science, 833 06 Bratislava, Slovakia;
Department of Biochemical Technology, Faculty of Chemical and Food Technology, Slovak University of Technology, 812 37 Bratislava, Slovakia
E-mail: elena.sebokova@savba.sk
Objective. The effect of dietary borage oil (rich in the gamma-linolenic acid [GLA]) on insulin sensitivity and lipid metabolism was compared with that of fish oil (rich in n-3 polyunsaturated
fatty acids [PUFAs]) in high fat (HF) diet-induced insulin resistance (IR) of rats.
Methods. Male Wistar rats were fed ad libitum for 3 weeks a standard laboratory chow (Controls) or high fat diet consisting of 70-cal % fat. In addition, a group of rats was fed high fat
(HF) diet where a part of saturated fat was replaced with fish oil as a source of n-3 PUFAs (HF+FO), or borage oil as a source of GLA (HF+GLA). In vivo insulin action was assessed by the
euglycemic hyperinsulinemic clamp. Glucose, insulin, free fatty acids (FFA), triglycerides (Tg) and glycerol levels in blood and tissue depots were also measured.
Results. Increased levels of Tg, FFA and glycerol in circulation after HF diet were accompanied by their raised accumulation in insulin sensitive tissues. FO feeding lowered the concentration
of all lipids in serum and prevented their accumulation in both tissues. On the other hand GLA supplementation into the high fat diet did not suppress increased levels of Tg, FFA and glycerol in
circulation and tissue depots as well. FO feeding significantly reduced HF diet-induced in vivo IR, while GLA supplementation did not improve the in vivo insulin sensitivity in HF diet induced
insulin resistance.
Conclusions: 1. Substitution of FO into the high fat diet led to an improvement of in vivo insulin action; 2. this insulin sensitizing effect of FO was accompanied by a decrease of
circulating Tg, FFA and glycerol levels in the postprandial state and by a lower lipid content in liver and skeletal muscle. 3. on the opposite, GLA treatment failed to improve in vivo insulin
action; and 4. was associated with an adverse effect on lipid levels both in circulation and tissue depots.
Key words: gamma-linolenic acid - HF diet – lipids – insulin action
ENDOCRINE REGULATIONS, Vol. 36, 143–149, 2002
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Helmut G. Hinghofer-Szalkay, Zoltán László, Daniela Jezova, Andreas Rössler, Bernd Haditsch, Karl Pilz, Herfried Passath, Hermann Scharfetter
Institute for Adaptive and Spaceflight Physiology, Graz, Austria (http://www.asm.at/iap);
Department of Physiology, Medical Faculty, University of Graz, Austria;
Csepeli Weiss Manfréd Hospital, Budapest, Hungary;
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia;
Institute for Electro- and Biomedical Engineering, Technical University Graz, Austria
Email: helmut.hinghofer@uni-graz.at
Objective. To answer the question if plasma hormone concentrations (plasma renin activity – PRA, vasopressin – pAVP, and aldosterone concentration) due to antiorthostatic
immobilization (8 days -6° head-down tilt bed rest – HDBR) are altered by oral salt load, we provided constant sodium supply during 4 days ambulatory conditions followed by 8 days
HDBR in 10 normotensive men.
Methods. A ‚low’ (LS: 143±10 mM) and ‚high’ (HS: 434±17 mM Na+/d excreted) sodium treatment were provided in randomized order, separated >= 1 mo. Before and at the
end of HDBR, hemodynamic variables and thoracic impedance were determined, and blood was taken for aldosterone and PRA, venous hematocrit, and plasma mass density. Extracellular fluid volume and pAVP
were determined every second day. Whole body electrical impedance spectroscopy was employed to assess changes in extracellular volume, hormone determinations were done with radioimmunoassay, mass
density measurements with the mechanical oscillator technique.
Results. Extracellular volume decreased with HDBR (LS: -4.0%, p=0.002; HS: -5.8%, p=0.018) without significant difference between salt treatments. Resting hormone levels were not altered by
HDBR, but pAVP was lower (5.5±0.1 pg/ml) in HS than in LS (7.2±0.3 pg/ml) as was plasma aldosterone (HS: 69±7 pg/ml, LS: 180±24 pg/ml). On the other hand, HDBR reduced extracellular volume by ?5%
irrespective of dietary sodium supply.
Conclusions. Our data support the hypothesis that hormonal activities are more affected by oral salt load than by simulated short-term space flight, and suggest that the reduction of
extracellular fluid volume due to head down bed rest is not influenced by moderate changes of dietary sodium supply.
Key words: Renal function – Extracellular volume – Bed rest – Immobilization – Salt intake – Vasopressin – Plasma renin activity – Aldosterone
– Bioelectrical impedance spectroscopy – Sodium excretion – Cardiovascular – Extracellular fluid volume
ENDOCRINE REGULATIONS, Vol. 36, 151–159, 2002
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Anna Goraca
Department of Experimental and Clinical Physiology, Institute of Physiology and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland
e-mail: agoraca@zdn.am.lodz.pl
Endothelin was isolated and identified in 1988 by Yanagisawa et al. The endothelin family consists of 21 amino acid isoforms endothelin-1, endothelin-2 and endothelin-3. Endothelin receptors are
present in many internal organs, e.g. heart, adrenals, kidneys, lung tissue, central nervous system. ET-1 is the main isoform which is synthetized in endothelial cells, muscular coat of arterial wall
as well as in heart, kidney and central nervous system. Endothelins affect multiple organ systems and are involved in the pathogenesis of many diseases. Moreover, ET-1 raises blood pressure, induces
vascular and myocardial hypertrophy. This paper is also concerned with endothelin receptor blockers which mediate relaxation of resistance arteries and, since they show a hypotensive effect, can
be useful in many cardiovascular diseases.
Key words: Endothelin – cardiovascular effects – minireview
ENDOCRINE REGULATIONS, Vol. 36, 161–167, 2002
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ENDOCRINE REGULATIONS, Vol. 36, 168, 2002
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ENDOCRINE REGULATIONS, Vol. 36, 169-189, 2002
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ENDOCRINE REGULATIONS, Vol. 36, 190-195, 2002
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