Variation of plasma ketones and free fatty acids during acute cold exposure in man

1965 ◽  
Vol 20 (1) ◽  
pp. 56-60 ◽  
Author(s):  
Peter G. Hanson ◽  
Robert E. Johnson
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Cold Exposure ◽  
Ketone Bodies ◽  
Control Period ◽  
Exposure Period ◽  
Nonesterified Fatty Acids ◽  
Acute Cold Exposure ◽  
Plasma Ffa ◽  
And Control

We have studied the magnitude of ketosis induced during acute cold exposure. Plasma and urinary ketone bodies and plasma free fatty acids (FFA) were followed in four healthy young men at rest during a 90-min period of seminude exposure to 0 C in still air. This period was followed by 4 hr of recovery at 25 C. Each subject served as his own control throughout an experimental sequence in which one cold-exposure and corresponding control period (25 C) were experienced each week for 3 successive weeks. The subjects were in a fasting state but with water ad libitum beginning 12 hr prior to the experiment. Light weight clothing was worn during recovery and control periods. The combined group data show a significant increase in plasma FFA during cold exposure as compared with similar control periods. Although true hyperketonemia or hyperketonuria did not develop, the levels of plasma ketones are elevated in the cold-exposure period of the first week. During the second and third week there is no difference between the cold and control plasma ketone concentration. The data suggest that FFA is mobilized as a metabolic substrate during cold exposure and that efficient peripheral utilization of the elevated plasma FFA concentration minimizes hyperketogenesis. ketone bodies; metabolism; nonesterified fatty acids Submitted on April 27, 1964

scholarly journals Effects of 3-hydroxybutyrate and free fatty acids on muscle protein kinetics and signaling during LPS-induced inflammation in humans: anticatabolic impact of ketone bodies

2018 ◽  
Vol 108 (4) ◽  
pp. 857-867 ◽  
Author(s):  
Henrik H Thomsen ◽  
Nikolaj Rittig ◽  
Mogens Johannsen ◽  
Andreas B Møller ◽  
Jens Otto Jørgensen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Acute Inflammation ◽  
Ketone Bodies ◽  
Muscle Protein ◽  
Initiation Factor ◽  
Whole Body ◽  
Protein Breakdown ◽  
Protein Kinetics ◽  
Nonesterified Fatty Acids

Abstract Background Acute inflammation, and subsequent release of bacterial products (e.g. LPS), inflammatory cytokines, and stress hormones, is catabolic, and the loss of lean body mass predicts morbidity and mortality. Lipid intermediates may reduce protein loss, but the roles of free fatty acids (FFAs) and ketone bodies during acute inflammation are unclear. Objective We aimed to test whether infusions of 3-hydroxybutyrate (3OHB), FFAs, and saline reduce protein catabolism during exposure to LPS and Acipimox (to restrict and control endogenous lipolysis). Design A total of 10 healthy male subjects were randomly tested 3 times, with: 1) LPS, Acipimox (Olbetam) and saline, 2) LPS, Acipimox, and nonesterified fatty acids (Intralipid), and 3) LPS, Acipimox, and 3OHB, during a 5-h basal period and a 2-h hyperinsulinemic, euglycemic clamp. Labeled phenylalanine, tyrosine, and urea tracers were used to estimate protein kinetics, and muscle biopsies were taken for Western blot analysis of protein metabolic signaling. Results 3OHB infusion increased 3OHB concentrations (P < 0.0005) to 3.5 mM and decreased whole-body phenylalanine-to-tyrosine degradation. Basal and insulin-stimulated net forearm phenylalanine release decreased by >70% (P < 0.005), with both appearance and phenylalanine disappearance being profoundly decreased. Phosphorylation of eukaryotic initiation factor 2α at Ser51 was increased in skeletal muscle, and S6 kinase phosphorylation at Ser235/236 tended (P = 0.074) to be decreased with 3OHB infusion (suggesting inhibition of protein synthesis), whereas no detectable effects were seen on markers of protein breakdown. Lipid infusion did not affect phenylalanine kinetics, and insulin sensitivity was unaffected by interventions. Conclusion During acute inflammation, 3OHB has potent anticatabolic actions in muscle and at the whole-body level; in muscle, reduction of protein breakdown overrides inhibition of synthesis. This trial was registered at clinicaltrials.gov as NCT01752348.

Starvation in the rat. II. Effect of age and obesity on protein sparing and fuel metabolism

1980 ◽  
Vol 239 (4) ◽  
pp. E277-E277 ◽  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Ketone Bodies ◽  
Blood Lipid ◽  
Blood Levels ◽  
Prolonged Starvation ◽  
Protein Sparing ◽  
Obese Rats ◽  
Protein Conservation ◽  
And Control

Sixteen-week-old control and obese rats survive longer than 8-wk-old control rats. In addition, unlike the 8-wk-old group, they conserve tissue RNA and protein. To evaluate the basis for this, the effects of starvation on circulating fuels and hormones and the urinary excretion of nitrogen and 3-methylhistidine (3MH) were compared in the three groups. Urinary nitrogen and 3MH diminished during prolonged starvation in 16-wk-old obese and control rats, suggesting that both groups are able to conserve protein and curtail muscle proteolysis. In contrast, urine nitrogen and 3MH did not decrease in 8-wk-old control rats. Protein conservation in the older rats was associated with diminished blood levels of alanine and increased levels of lipid fuels, ketone bodies, and free fatty acids. Although ketone bodies and free fatty acids were also increased during the first few days of starvation in 8-wk-old rats, there was no evidence of protein sparing. In all groups, as fat stores became exhausted terminally, blood lipid levels decreased and protein catabolism increased. Starvation caused insulin to decrease to comparable levels in all rats; however, minimal levels were reached later in the older groups. Thyroxine and triiodothyronine (T3) decreased during the fast in both control groups; however, T3 did not decrease in the obese rats. These findings support the contention that the conservation of protein during prolonged starvation requires the continued availability of lipid fuels. The role of insulin and thyroid hormone in modulating these adaptations is unclear.

Source of plasma free fatty acids in dogs receiving fat emulsion and heparin

1963 ◽  
Vol 204 (4) ◽  
pp. 691-695 ◽  
Author(s):  
H. C. Meng ◽  
B. Edgren
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Lipolytic Activity ◽  
Blocking Agent ◽  
Fat Emulsion ◽  
Similar Reduction ◽  
Plasma Free Fatty Acids ◽  
Fat Infusion ◽  
Plasma Ffa ◽  
Slight Rise

Unanesthetized dogs were given either 3.0 g fat/kg as a 20% fat emulsion or heparin (2 mg/kg) intravenously or both. Plasma free fatty acids (FFA) and lipolytic activity were determined at intervals. In some experiments hexamethonium (5 mg/kg), a sympathetic ganglionic blocking agent, was administered intravenously either before or after fat or heparin. In fasting dogs fat infusion produced a moderate and heparin caused a slight rise in plasma FFA. Heparin given during lipemia produced a marked elevation of plasma FFA. The plasma lipolytic activity was increased after fat emulsion or heparin. Hexamethonium reduced the fasting plasma FFA about 70% or 0.40–0.6 mEq/liter. A similar reduction of plasma FFA also was observed when hexamethonium was administered during fat infusion or after heparin. Hexamethonium did not affect the increase in plasma lipolytic activity following the administration of fat emulsion or heparin. It seems probable that the increase in plasma FFA observed after intravenous infusion of fat emulsion or heparin is mainly due to the result of intravascular lipolysis.

EFFECT OF COLD EXPOSURE ON RESPIRATORY C14O2 PRODUCTION DURING INFUSION OF ALBUMIN-BOUND PALMITATE-1-C14 IN WHITE RATS

1961 ◽  
Vol 39 (2) ◽  
pp. 219-224 ◽  
Author(s):  
Roberto Masironi ◽  
Florent Depocas
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Cold Exposure ◽  
Carbohydrate Utilization ◽  
White Rats ◽  
Constant Rate ◽  
Oxidation Of Glucose ◽  
Fasted Rats

Albumin palmitate-1-C14 complex was infused at a constant rate through a carotid cannula (inserted 5–7 days earlier) into otherwise intact non-fasted rats in environments at 30° or 6 °C, after acclimation to 30° or 6 °C. At 6 °C, both warm- and cold-acclimated rats similarly exhaled as CI4O2 a larger proportion of the injected C14 and gave lower terminal amounts of C14 in the extracted free fatty acids (F.F.A.) of plasma than at 30 °C. These results indicate that plasma F.F.A. serve as substrate for cold-thermogenesis. Also, increased turnover and oxidation of F.F.A. are not always inversely related to carbohydrate utilization but may be increased under conditions which result in concomitantly higher rates of turnover and oxidation of glucose.

Free fatty acids normalize a rosiglitazone-induced visfatin release

2006 ◽  
Vol 291 (5) ◽  
pp. E885-E890 ◽  
Author(s):  
Dominik G. Haider ◽  
Friedrich Mittermayer ◽  
Georg Schaller ◽  
Michaela Artwohl ◽  
Sabina M. Baumgartner-Parzer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Term Treatment ◽  
Double Blind ◽  
Lipid Infusion ◽  
Major Mechanism ◽  
Insulin Mimetic ◽  
Long Term Treatment ◽  
Plasma Ffa

The detrimental effect of elevated free fatty acids (FFAs) on insulin sensitivity can be improved by thiazolidinediones (TZDs) in patients with type 2 diabetes mellitus. It is unknown whether this salutary action of TZD is associated with altered release of the insulin-mimetic adipocytokine visfatin. In this study, we investigated whether visfatin concentrations are altered by FFA and TZD treatment. In a randomized, double-blind, placebo-controlled, parallel-group study 16 healthy volunteers received an infusion of triglycerides/heparin to increase plasma FFA after 3 wk of treatment with rosiglitazone (8 mg/day, n = 8) or placebo ( n = 8), and circulating plasma visfatin was measured. As a corollary, human adipocytes were incubated with synthetic fatty acids and rosiglitazone to assess visfatin release in vitro. The results were that rosiglitazone treatment increased systemic plasma visfatin concentrations from 0.6 ± 0.1 to 1.7 ± 0.2 ng/ml ( P < 0.01). Lipid infusion caused a marked elevation of plasma FFA but had no effect on circulating visfatin in controls. In contrast, elevated visfatin concentrations in subjects receiving rosiglitazone were normalized by lipid infusion. In isolated adipocytes, visfatin was released into supernatant medium by acute addition and long-term treatment of rosiglitazone. This secretion was blocked by synthetic fatty acids and by inhibition of phosphatidylinositol 3-kinase or Akt. In conclusion, release of the insulin-mimetic visfatin may represent a major mechanism of metabolic TZD action. The presence of FFA antagonizes this action, which may have implications for visfatin bioactivity.

Central and peripheral adrenoceptors affect glucose, free fatty acids, and insulin in exercising rats

1988 ◽  
Vol 255 (4) ◽  
pp. R547-R556 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
L. Benthem
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Blood Samples ◽  
Beta Adrenoceptor ◽  
Plasma Ffa ◽  
Glucose Plasma ◽  
Exercise Induced ◽  
Counter Current ◽  
Lateral Area

The effects of intravenously and intrahypothalamically administered alpha- and beta-adrenoceptor antagonists on exercise-induced alterations in blood glucose, plasma free fatty acids (FFA), and insulin were investigated in rats. Exercise consisted of strenuous swimming against a counter current for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter. Intravenous administration of the alpha-blocker phentolamine led to a reduction in glucose and a substantial increase in insulin levels. Infusion of phentolamine through permanent bilateral cannulas into either the ventromedial or lateral area of the hypothalamus (VMH and LHA, respectively) completely prevented the increase in glucose while the decline in insulin was unaffected. Infusion of phentolamine into the VMH caused much higher plasma FFA levels than in controls. The beta-blocker timolol given intravenously caused a delayed increase in glucose and prevented the increase in FFA. Infusion of timolol into either VMH or LHA caused a delay in the increase in both glucose and FFA. The results suggest that 1) both peripheral and hypothalamic adrenoceptors are involved in energy metabolism during exercise and 2) FFA, glucose, and insulin concentrations in blood are independently regulated by VMH and LHA.

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