scholarly journals The metabolism of glucose, acetate, palmitate, stearate and oleate in pigs

1970 ◽  
Vol 24 (3) ◽  
pp. 705-716 ◽  
Author(s):  
C. P. Freeman ◽  
D. E. Noakes ◽  
E. F. Annison

1. Isotope dilution techniques were used to measure the rates of entry and oxidation of glucose, acetate, palmitate, stearate and oleate in fed and fasted (16 h) pigs.2. Glucose entry rates measured in eight fed and five fasted (16 h) pigs were 20.6 and 8.0 mg/min per kg0.75 (mean values) respectively. The entry rates in fed pigs were lower than the calculated rates of glucose uptake from the alimentary tract, and the validity of glucose entry rates determined under these conditions is discussed.3. Acetate entry rates were unrelated to the fibre content of the diet, and acetate produced from endogenous metabolism was the main contributor to total acetate production.4. Increased rates of entry and oxidation of palmitate, stearate and oleate were observed in fasted pigs.5. Glucose production in fasted pigs was inhibited by raising the concentration of blood glucose. Infusion of insulin in the fed pig caused a decrease in glucose production and a simultaneous reduction in the mobilization of free fatty acids. When blood glucose concentrations fell below about 55 mg/100 ml the release of free fatty acid into the circulation was restored.

2008 ◽  
Vol 86 (9) ◽  
pp. 643-649 ◽  
Author(s):  
Thomas P. Johnston ◽  
David J. Waxman

Poloxamer 407 (P-407) is a copolymer surfactant that induces a dose-controlled dyslipidemia in both mice and rats. Human macrophages cultured with P-407 exhibit a concentration-dependent reduction in cholesterol efflux to apolipoprotein A1 (apoA1) linked to downregulation of the ATP-binding cassette transporter A1 (ABCA1). Activators of peroxisome proliferator-activated receptor gamma (PPARγ), as well as PPARα, increase expression of liver X receptor alpha (LXRα) in macrophages and promote the expression of ABCA1, which, in turn, mediates cholesterol efflux to apoA1. The present study investigated whether P-407 interferes with this signaling pathway. A transactivation assay was used to evaluate whether P-407 can either activate or inhibit the transcriptional activity of PPARγ. Because thiazolidinedione drugs (PPARγ agonists) improve glycemic control in type 2 diabetes by reducing blood glucose concentrations, P-407 was also evaluated for its potential to alter plasma insulin and blood glucose concentrations in wild-type (C57BL/6) and PPARγ-deficient mice. Additionally, because thiazolidinediones attenuate release of free fatty acids (FFAs) from adipocytes and, consequently, decrease circulating plasma levels of FFAs, plasma concentrations of circulating FFAs were also determined in P-407-treated mice. P-407 was unable to modulate PPARγ activity in cell-based transactivation assays. Furthermore, P-407 did not perturb plasma insulin and blood glucose concentrations after administration to mice. However, by an as yet unidentified mechanism, P-407 caused a significant increase in the serum concentration of FFAs in mice beginning 3 h after administration and lasting more than 24 h postdosing. It is concluded that P-407 does not interfere with the functional activity of PPARγ after administration to mice.


1982 ◽  
Vol 204 (3) ◽  
pp. 749-756 ◽  
Author(s):  
M C Sugden ◽  
D I Watts ◽  
C E Marshall

1. Injection of adrenaline into 24 h-starved rats caused a 69% decrease in blood [ketone-body] (3-hydroxybutyrate plus acetoacetate), accompanied by a decreased [3-hydroxybutyrate]/[acetoacetate] ratio. Blood [glucose] and [lactate] increased, but [alanine] was unchanged. 2. Adrenaline also decreased [ketone-body] after intragastric feeding of both long- and medium-chain triacylglycerol. The latter decrease was observed after suppression of lipolysis with 5-methylpyrazole-3-carboxylic acid, indicating that the antiketogenic action of adrenaline was not dependent on the chain length of the precursor fatty acid. 3. The actions of adrenaline to decrease blood [ketone-body] and to increase blood [glucose] were not observed after administration of 3-mercaptopicolinate, an inhibitor of gluconeogenesis. This suggests that these effects of the hormone are related. 4. The possible clinical significance of the results is discussed with reference to the restricted ketosis often observed after surgical or orthopaedic injury.


2008 ◽  
Vol 53 (No. 12) ◽  
pp. 515-522 ◽  
Author(s):  
N. Aldai ◽  
M.E.R. Dugan ◽  
A.I. Nájera ◽  
K. Osoro

Levels of n-6 and n-3 PUFAs, including those with 20 and 22 carbon-chains, in concentrate-fed Asturiana de los Valles (AV) yearling bulls with and without the double muscling gene <I>(mh/mh</I> = 24, <I>mh</I>/+ = 26, +/+ = 25) were measured to examine if this gene influences the pattern of PUFA deposition in different adipose tissues. Fatty acid compositions of muscle tissue (<I>longissimus thoracis</I>) and intermuscular and subcutaneous adipose tissues were determined by gas chromatography. The composition of intramuscular fat was unique compared to the other two adipose tissues which were similar in composition. In general, n-6 and n-3 fatty acid elongation and desaturation products were affected by AV genotype and this effect was most evident in n-3 PUFAs of the intramuscular fat of <I>mh/mh</I> (n-6/n-3 = 11.8 and 18:2n-6/18:3n-3 = 25.3) compared to <I>mh</I>/+ and +/+ animals (mean values of n-6/n-3 = 9.86 and 18:2n-6/18:3n-3 = 15.5). PUFA elongation and desaturation end products did not accumulate to any great extent in intermuscular and subcutaneous adipose tissues. Beef from <I>mh/mh</I> cattle showed greater deposition rates of n-3 elongation and desaturation products but their absolute content of total n-3 fatty acids was lower (21 mg/100 g meat) in comparison with <I>mh</I>/+ and +/+ cattle (mean value of 25 mg/100 g meat).


1991 ◽  
Vol 261 (3) ◽  
pp. E304-E311 ◽  
Author(s):  
M. Walker ◽  
G. R. Fulcher ◽  
C. F. Sum ◽  
H. Orskov ◽  
K. G. Alberti

The purpose of this study was to examine the effect of physiological plasma nonesterified fatty acid (NEFA) levels on insulin-stimulated forearm and whole body glucose uptake and substrate oxidation during euglycemia and hyperglycemia. Seven healthy men received Intralipid and heparin for 210 min in two studies, with saline as control in two further studies. Insulin (0.05 U.kg-1.h-1) was infused from 60 min, and euglycemia was maintained during lipid (EL) and control (EC) studies, and hyperglycemia was maintained in the other studies (HL and HC). Forearm NEFA uptake was comparable in the lipid studies (+61 +/- 10 and +52 +/- 8 nmol.100 ml forearm-1.min-1, EL and HL) and was suppressed in the controls. With Intralipid, forearm glucose uptake decreased during euglycemia but not during hyperglycemia (+3.85 +/- 0.34 vs. +3.34 +/- 0.25 mumol.100 ml forearm-1.min-1, EC vs. EL, P less than 0.02), with comparable changes in whole body glucose uptake. Glucose oxidation and forearm alanine release decreased with Intralipid at both blood glucose levels, with no significant change in the rates of nonoxidative glucose disposal. These observations support the operation of the glucose-fatty acid cycle at physiological plasma NEFA levels at both blood glucose concentrations, but this was associated with a decrease in peripheral insulin sensitivity only during euglycemia.


Diabetes ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 580-588 ◽  
Author(s):  
M. R. Taskinen ◽  
T. Sane ◽  
E. Helve ◽  
S. L. Karonen ◽  
E. A. Nikkila ◽  
...  

Diabetes ◽  
1989 ◽  
Vol 38 (5) ◽  
pp. 580-588 ◽  
Author(s):  
M.-R. Taskinen ◽  
T. Sane ◽  
E. Helve ◽  
S.-L. Karonen ◽  
E. A. Nikkila ◽  
...  

2021 ◽  
Author(s):  
Lucy A. Ochola ◽  
Eric M. Guantai

Hyperglycemia is the elevation of blood glucose concentrations above the normal range. Prolonged uncontrolled hyperglycemia is associated with serious life-threatening complications. Hyperglycemia arises from an imbalance between glucose production and glucose uptake and utilization by peripheral tissues. Disorders that compromise pancreatic function or affect the glucose counter-regulatory hormones cause hyperglycemia. Acute or serious illness or injury may also bring about hyperglycemia, as can many classes of drugs. Metformin lowers blood glucose levels by inhibiting the production of glucose by the liver whilst enhancing uptake of circulating glucose and its utilization in peripheral tissues such as muscle and adipose tissue. Metformin suppresses hepatic gluconeogenesis by inhibiting mitochondrial respiration and causing a reduction of cellular ATP levels. Metformin may also modulate the gut-brain-liver axis, resulting in suppression of hepatic glucose production. Metformin also opposes the hyperglycemic action of glucagon and may ameliorate pancreatic cell dysfunction associated with hyperglycemia. Metformin is therefore recommended for use in the prevention of hyperglycemia, including drug-induced hyperglycemia, in at risk patients. The benefits of metformin in the prevention of hyperglycemia are unmatched despite its contraindications.


1976 ◽  
Vol 29 (2) ◽  
pp. 33 ◽  
Author(s):  
N D Costa ◽  
GH Mclntosh ◽  
AM Snoswell

The production of endogenous acetate by the liver has been investigated in lactating ewes using animals with indwelling arterial, and portal and hepatic venous cannulae. The capacity of the liver to produce acetate from acetyl-CoA in vitro has also been examined using homogenates prepared from liver biopsy samples. Mean arterial, portal and hepatic venous blood acetate concentrations in four ewes at 4 weeks lactation were 0'40, 1�00 and 1�46 mM respectively. The mean exogenous and endogenous acetate production rates were 56 and 54 mmol/h respectively, giving a total of 110 mrnol/h. The mean portal-hepatic venous difference in free fatty acid concentration was 81 11M. Converting this uptake of free fatty acids by the liver (based on palmitate as a standard) to 2-carbon equivalents, the acetate produced accounted for 70 % of the fatty acids taken up. The correlation coefficient (r2) between uptake of free fatty acids and production of acetate by the liver was o� 83 (P < O� 01),


Sign in / Sign up

Export Citation Format

Share Document