34-OR: Maladaptive Increases in Skeletal Muscle Ketone Body Oxidation Contribute to Dysglycemia in Mice Subjected to Experimental Obesity

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 34-OR
Author(s):  
RAMI AL BATRAN ◽  
KESHAV GOPAL ◽  
JADIN J. CHAHADE ◽  
JOHN R. USSHER
Keyword(s):  
PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e98109 ◽  
Author(s):  
Maria Guitart ◽  
Óscar Osorio-Conles ◽  
Thais Pentinat ◽  
Judith Cebrià ◽  
Judit García-Villoria ◽  
...  

2011 ◽  
Vol 57 (1) ◽  
pp. 93-98
Author(s):  
Ryota Narishima ◽  
Masahiro Yamasaki ◽  
Saki Yoshida ◽  
Shinya Hasegawa ◽  
Tetsuya Fukui

1982 ◽  
Vol 48 (3) ◽  
pp. 549-563 ◽  
Author(s):  
D. W. Pethick ◽  
D. B. Lindsay

1. A combination of isotope-dilution and arteriovenous-difference techniques was used to determine the significance of ketones to energy homoeostasis in fasted pregnant ewes.2. There was incomplete interconversion of D(−) 3-hydroxybutyrate (3HB) and acetoacetate (AcAc) and therefore neither entry rate nor oxidation of total ketone bodies could be estimated by assuming circulating ketone bodies represent a single metabolic compartment. Total ketone body metabolism was satisfactorily summarized using a three-compartment model. In fasted pregnant ewes the mean entry rate of total ketones was 1 mmol/h per kg body-weight and of the ketones entering the circulation 87% were promptly oxidized to carbon dioxide accounting for 30% of the total COa production.3. Ketone bodies are readily utilized by hind-limb skeletal muscle such that if completely oxidized, 18±4 and 48±3% of the oxygen utilized could be accounted for in fed and fasted pregnant ewes respectively. For both 3HB and AcAc there was a hyperbolic relationship between utilization and arterial concentration. The apparent Michaelis constant (Km) values were 0·55 and 1–42 mM respectively and the maximum velocity (Vmax) 2·9 and 5·6 mmol/h per kg muscle. The arterial concentration of AcAc is always below the Km value and this limits the utilization rate. The D(−) 3HB concentration, however, may surpass that required for maximum utilization and ketoacidosis may be a consequence of this.4. A two-compartment model was used to analyse ketone body metabolism by hind-limb skeletal muscle. The results suggested substantial intercon version and production of AcAc and 3HB.5. The pregnant uterus utilized 3HB which if completely oxidized accounted for 12±2 (fed) and 25±4 (fasted) % of its O2 consumption. At least 64% of the net 3HB utilized was oxidized. AcAc was not utilized in significant quantities.


1990 ◽  
Vol 37 (3) ◽  
pp. 421-429 ◽  
Author(s):  
HAJIME OHMORI ◽  
KOICHI KAWAI ◽  
KAMEJIRO YAMASHITA
Keyword(s):  

2016 ◽  
Vol 30 (5) ◽  
pp. 1976-1986 ◽  
Author(s):  
Kristoffer Svensson ◽  
Verena Albert ◽  
Bettina Cardel ◽  
Silvia Salatino ◽  
Christoph Handschin
Keyword(s):  

1985 ◽  
Vol 249 (2) ◽  
pp. E131-E136 ◽  
Author(s):  
R. Nosadini ◽  
A. Avogaro ◽  
L. Sacca ◽  
C. Vigorito ◽  
S. de Kreutzenberg ◽  
...  

Although the liver is considered the major source of ketone bodies (KB) in humans, these compounds may also be formed by nonhepatic tissues. To study this aspect further, 3-[14C]hydroxybutyrate (BOH) or [3-14C]acetoacetate (AcAc) were constantly infused after a priming dose and contemporaneous arterial and venous samples were taken at splanchnic, heart, kidney, and leg sites in eight normal subjects (N) undergoing diagnostic catheterization and at the forearm site in five normal and six ketotic diabetic (D) subjects. After 70 min of infusion, tracer and tracee levels of AcAc and BOH reached a steady state in the artery and vein in both normal and diabetic subjects. The venous-arterial (V-A) difference at the forearm step for cold KB was negligible both in normal and diabetic subjects, whereas for labeled KB it was approximately 10-fold higher in diabetic subjects (V-A AcAc, -31 +/- 7 and -270 +/- 34 dpm/ml in N and D, respectively; V-A BOH, -38 +/- 6 and -344 +/- 126 dpm/ml in N and D, respectively). We assumed that the V-A difference in tracer concentration was consistent with dilution of the tracer by newly synthesized tracee inside the muscle and calculated that the forearm muscle produces KB at a rate of 16.2 +/- 3.3 mumol/min in D and 0.9 +/- 0.9 mumol/min in N. These findings can be accounted for by the hypothesis that the disappearance flux of KB from circulation was replaced by an equivalent flux of KB entering the vein at the muscle step in D but not in N. Moreover, in N KB were not only produced but also utilized by the splanchnic area (39 +/- 9 mumol/min).(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
D. E. Philpott ◽  
A. Takahashi

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.


Author(s):  
Joachim R. Sommer ◽  
Nancy R. Wallace

After Howell (1) had shown that ruthenium red treatment of fixed frog skeletal muscle caused collapse of the intermediate cisternae of the sarcoplasmic reticulum (SR), forming a pentalaminate structure by obi iterating the SR lumen, we demonstrated that the phenomenon involves the entire SR including the nuclear envelope and that it also occurs after treatment with other cations, including calcium (2,3,4).From these observations we have formulated a hypothesis which states that intracellular calcium taken up by the SR at the end of contraction causes the M rete to collapse at a certain threshold concentration as the first step in a subsequent centrifugal zippering of the free SR toward the junctional SR (JSR). This would cause a) bulk transport of SR contents, such as calcium and granular material (4) into the JSR and, b) electrical isolation of the free SR from the JSR.


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