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Biomedical subjects

B Ljung

Publications and source records attributed to B Ljung.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

A proteome analysis of livers from obese (ob/ob) mice treated with the peroxisome proliferator WY14,643.

The PPAR (peroxisome proliferator activated receptor) transcription factors are ligand-activated receptors which regulate genes involved in lipid metabolism and homeostasis. PPARalpha is preferentially expressed in the liver and PPARgamma preferentially in adipose tissue. Activation of PPARalpha leads to peroxisome proliferation in rodents and increased beta-oxidation of fatty acids. PPARgamma-activation leads to adipocyte differentiation and improved insulin signaling of mature adipocytes. Both of these PPAR receptors are potential targets for treatment of dyslipidemia in man. Studies by others using a proteomics approach have characterized the effects of PPARalpha agonists in livers from lean healthy mice. However, we wanted to map the effects of a therapeutic dose of a PPARalpha agonist in a disease model of insulin resistance and diabetes, the obese diabetic ob/ob mouse, by proteomics. Therefore, ob/ob mice, which have highly elevated levels of plasma triglycerides, glucose and insulin, were treated for one week with WY14,643 (180 micromol/kg/day), a well-characterized selective PPARalpha agonist. Plasma triglycerides, glucose and insulin levels were determined and we found significant therapeutic effects on triglycerides and glucose levels. The liver protein compositions were investigated by high-resolution two-dimensional gel electrophoresis which showed that WY14,643 produced up-regulation of at least 16 spots. These were identified by mass spectrometry and 14 spots were found to be components of the peroxisomal fatty acid metabolism. Thus, WY14,643 at a therapeutic dose, caused induction of peroxisomal fatty acid beta-oxidation in obese diabetic mice.

Animals↗
PubMedDate not supplied

Separation of antihypertensive from ganglioplegic effects of felodipine in the cat.

The effects of felodipine on sympathetic ganglionic transmission and on the effector responses of two muscle models were studied. In anesthetized cats we established what injected dose and plasma levels of this selectively vasodilating dihydropyridine were necessary for the neural and for the primary hypotensive effects on arterial blood pressure in vivo. Felodipine in cats reduced mean arterial pressure at a dose of 0.010 mumol/kg i.v., corresponding to a plasma concentration of 10 nmol/L. A 15-25-fold higher dose, or plasma concentration, was required to produce a significant reduction in the amplitude of the sympathetic postganglionic action potential (PAP). The latencies of the PAPs remained constant. Felodipine in vitro did not attenuate the neurogenic response of the nictitating membrane. However, the spontaneous activity, as well as the neurogenic response of the portal vein, was inhibited by felodipine in nanomolar concentrations. Felodipine at the highest dose caused a small but significant attenuation of the postganglionic nictitating membrane response in vivo. This reduction was of insufficient magnitude to account alone for the diminution of the response to preganglionic stimulation. We conclude that felodipine in low concentrations reduces blood pressure by a direct relaxation of vascular smooth muscle, while, in addition, at high concentrations a partial ganglionic blockade may be induced.

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