Effect of elevated plasma ketones on cardiac efficiency

2021 ◽  
Vol 242 ◽  
pp. 163
Author(s):  
Carolina Solis-Herrera ◽  
Yuejuan Qin ◽  
Henri Honka ◽  
Goeffrey Clarke ◽  
Curtis Triplitt ◽  
...  
1985 ◽  
Vol 53 (01) ◽  
pp. 157-157 ◽  
Author(s):  
Czeslaw S Ciemiewski ◽  
Malgorzata Wilczynska ◽  
Wieslaw Augustyniak ◽  
Maria A Kowalska

1985 ◽  
Vol 53 (01) ◽  
pp. 005-007 ◽  
Author(s):  
I Pabinger-Fasching ◽  
K Lechner ◽  
H Niessner ◽  
P Schmidt ◽  
E Balzar ◽  
...  

SummaryIn patients with severe nephrotic syndrome determinations of plasma protein C : Ag levels (8 patients: 5 adults, 3 children) and protein C activity (3 out of 8 patients) revealed significantly elevated plasma protein C concentrations. Furthermore we observed a significant inverse correlation of protein C : Ag to AT III : Ag levels. No protein C : Ag could be detected in the urine of two patients studied. We conclude from our data, that changes of plasma protein C do not contribute to the high thrombotic tendency in nephrotic syndrome.


1984 ◽  
Vol 52 (02) ◽  
pp. 183-187 ◽  
Author(s):  
D A Lane ◽  
H Ireland ◽  
S Wolff ◽  
E Ranasinghe ◽  
J Dawes

SummaryDuring the platelet release reaction β-thromboglobulin (βTG), platelet factor 4 (PF4) and thrombospondin (TSP) are released from the platelet into plasma and assays of these proteins can be used to monitor in vivo platelet activation. We have assessed their relative merits as markers of the in vivo platelet α-granule release reaction in a number of patient groups which have previously been shown to have elevated plasma βTG and/or PF4 levels. It is concluded that in diseases or conditions not complicated by its reduced clearance, βTG is the most sensitive marker of in vivo platelet α-granule release. However, the TSP assay may be the least ambiguous when monitoring the platelet α-granule release reaction in patients with renal failure who are undergoing haemodialysis with heparin anticoagulation. Under these circumstances plasma βTG, but not PF4 or TSP, levels are elevated because of impaired renal catabolism, and the presence of a heparin-releasable reservoir of PF4 on the endothelium complicates the use of the PF4 assay. In liver failure none of these assays may accurately reflect platelet α-granule release because of impaired hepatic or renal elimination of the proteins.


Author(s):  
Ada Admin ◽  
Michelle Carey ◽  
Eric Lontchi-Yimagou ◽  
William Mitchell ◽  
Sarah Reda ◽  
...  

Hyperglycemia is a potent regulator of endogenous glucose production (EGP). Loss of this ‘glucose effectiveness’ is a major contributor to elevated plasma glucose concentrations in type 2 diabetes (T2D). ATP-sensitive potassium channels (K<sub>ATP</sub> channels) in the central nervous system (CNS) have been shown to regulate EGP in humans and rodents. We examined the contribution of central K<sub>ATP</sub> channels to glucose effectiveness. Under fixed hormonal conditions (‘pancreatic clamp’ studies), hyperglycemia suppressed EGP by ~50% in both non-diabetic humans and normal Sprague Dawley rats. By contrast, antagonism of K<sub>ATP</sub> channels with glyburide significantly reduced the EGP-lowering effect of hyperglycemia in both humans and rats. Furthermore, the effects of glyburide on EGP and gluconeogenic enzymes in rats were abolished by intracerebroventricular (ICV) administration of the KATP channel agonist diazoxide. These findings indicate that about half of EGP suppression by hyperglycemia is mediated by central K<sub>ATP</sub> channels. These central mechanisms may offer a novel therapeutic target for improving glycemic control in T2D.


Diabetes ◽  
1992 ◽  
Vol 41 (9) ◽  
pp. 1160-1164 ◽  
Author(s):  
J. C. Levy ◽  
J. L. Morton ◽  
M. Davenport ◽  
A. Beloff-Chain ◽  
R. C. Turner

2000 ◽  
Vol 25 (1) ◽  
pp. 68-78 ◽  
Author(s):  
Craig S. Ballantyne ◽  
Stuart M. Phillips ◽  
Jay R. Macdonald ◽  
Mark A. Tarnopolsky ◽  
J. Duncan Macdougall

We examined the effects of androstenedione supplementation on the hormonal profile of 10 males and its interaction with resistance exercise. Baseline testosterone, luteinizing hormone, estradiol, and androstenedione concentrations were established by venous sampling at 3 hr intervals over 24 hr. Subjects ingested 200 mg of androstenedione daily for 2 days, with second and third day blood samples. Two weeks later, they ingested androstenedione or a placebo for 2 days, in a double-blind, cross-over design. On day 2, they performed heavy resistance exercise with blood sampled before, after, and 90 min post. The supplement elevated plasma androstenedione 2-3-fold and luteinizing hormone ∼70% but did not alter testosterone concentration. Exercise elevated testosterone, with no difference between conditions. Exercise in the supplemented condition significantly elevated plasma estradiol by ∼83% for 90 min. Androstenedione supplementation, thus, is unlikely to provide male athletes with any anabolic benefit and, with heavy resistance exercise, elevates estrogen. Key Words: testosterone, luteinizing hormone, estradiol, fluid shifts, resistance exercise


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