scholarly journals Effect of dietary fish oil on blood levels of free fatty acids, ketone bodies and triacylglycerol in humans

Lipids ◽  
1994 ◽  
Vol 29 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Pieter C. Dagnelie ◽  
Trinette Rietveld ◽  
G. Roelof Swart ◽  
Theo Stijnen
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Free Fatty Acids ◽  
Ketone Bodies ◽  
Blood Levels ◽  
Dietary Fish

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.

scholarly journals Influence of Dietary Fish Oil on Conjugated Linoleic Acid and Other Fatty Acids in Milk Fat from Lactating Dairy Cows

2000 ◽  
Vol 83 (11) ◽  
pp. 2620-2628 ◽  
Author(s):  
D.C. Donovan ◽  
D.J. Schingoethe ◽  
R.J. Baer ◽  
J. Ryali ◽  
A.R. Hippen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Fish Oil ◽  
Dairy Cows ◽  
Conjugated Linoleic Acid ◽  
Milk Fat ◽  
Lactating Dairy Cows ◽  
Dietary Fish

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.

Effect of dietary fish oil on biohydrogenation of fatty acids and milk fatty acid content in cows

2003 ◽  
Vol 77 (1) ◽  
pp. 165-179 ◽  
Author(s):  
K. J. Shingfield ◽  
S. Ahvenjärvi ◽  
V. Toivonen ◽  
A. Ärölä ◽  
K. V. V. Nurmela ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Milk Fat ◽  
Fatty Acid Content ◽  
Sampling Technique ◽  
Lactating Cows ◽  
Dietary Fish ◽  
Total Fatty Acids ◽  
In Trans ◽  
Second Period

AbstractMechanisms underlying milk fat conjugated linoleic acid (CLA) responses to supplements of fish oil were investigated using five lactating cows each fitted with a rumen cannula in a simple experiment consisting of two consecutive 14-day experimental periods. During the first period cows were offered 18 kg dry matter (DM) per day of a basal (B) diet formulated from grass silage and a cereal based-concentrate (0·6 : 0·4; forage : concentrate ratio, on a DM basis) followed by the same diet supplemented with 250 g fish oil per day (FO) in the second period. The flow of non-esterified fatty acids leaving the rumen was measured using the omasal sampling technique in combination with a triple indigestible marker method based on Li-Co-EDTA, Yb-acetate and Cr-mordanted straw. Fish oil decreased DM intake and milk yield, but had no effect on milk constituent content. Milk fat trans-11 C18:1, total trans-C18 : 1, cis-9 trans-11 CLA, total CLA, C18 : 2(n-6) and total C18 : 2content were increased in response to fish oil from 1·80, 4·51, 0·39, 0·56, 0·90 and 1·41 to 9·39, 14·39, 1·66, 1·85, 1·25 and 4·00 g/100 g total fatty acids, respectively. Increases in the cis-9, trans-11 isomer accounted for proportionately 0·89 of the CLA response to fish oil. Furthermore, fish oil decreased the flow of C18 : 0(283 and 47 g/day for B and FO, respectively) and increased that of trans-C18 : 1fatty acids entering the omasal canal (38 and 182 g/day). Omasal flows of trans-C18 : 1acids with double bonds in positions from delta-4 to -15 inclusive were enhanced, but the effects were isomer dependent and primarily associated with an increase in trans-11 C18 : 1 leaving the rumen (17·1 and 121·1 g/day for B and FO, respectively). Fish oil had no effect on total (4·36 and 3·50 g/day) or cis-9, trans-11 CLA (2·86 and 2·08 g/day) entering the omasal canal. Flows of cis-9, trans-11 CLA were lower than the secretion of this isomer in milk. Comparison with the transfer of the trans-9, trans-11 isomer synthesized in the rumen suggested that proportionately 0·66 and 0·97 of cis-9, trans-11 CLA was derived from endogenous conversion of trans-11 C18 : 1in the mammary gland for B and FO, respectively. It is concluded that fish oil enhances milk fat cis-9, trans-11 CLA content in response to increased supply of trans-11 C18:1that arises from an inhibition of trans-C18 : 1reduction in the rumen.

Effect of dietary fish oil on milk yield, fatty acids content and serum metabolic profile in dairy cows

2010 ◽  
Vol 95 (4) ◽  
pp. 512-522 ◽  
Author(s):  
R. Kupczyński ◽  
M. Szołtysik ◽  
W. Janeczek ◽  
J. Chrzanowska ◽  
S. Kinal ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fish Oil ◽  
Dairy Cows ◽  
Milk Yield ◽  
Metabolic Profile ◽  
Dietary Fish

scholarly journals A Clinical Case of Clozapine-Induced Fatal Diabetic Ketoacidosis

2016 ◽  
Vol 7 ◽  
pp. CMPsy.S30532
Author(s):  
Eric Romney ◽  
Vinay J. Nagaraj ◽  
Amie Kafer
Keyword(s):  
Fatty Acids ◽  
Weight Gain ◽  
Free Fatty Acids ◽  
Diabetic Ketoacidosis ◽  
Ketone Bodies ◽  
Pancreatic Beta Cell ◽  
Metabolic Effects ◽  
Psychotic Symptoms ◽  
Life Threatening ◽  
Altered Metabolism

Introduction Clozapine, a second generation medication, has become the atypical antipsychotic drug of choice for refractory or treatment-resistant schizophrenia. In addition to the high risk of agranulocytosis and seizures, clozapine treatment is increasingly associated with significant metabolic effects, such as hyperglycemia, central weight gain and adiposity, hypertriglyceridemia, and elevated low-density lipoprotein cholesterol. A potentially life-threatening complication of altered metabolism is diabetic ketoacidosis (DKA). This report details a case of fatal DKA in a schizophrenic patient undergoing treatment with clozapine. Case Description An African–American male in his 20s with a medical history significant for schizophrenia was presented to the psychiatric inpatient ward with severe paranoid thoughts and aggressive behavior. After trials of risperidone, olanzapine, and haloperidol—all of which failed to adequately control his psychotic symptoms—clozapine titration was initiated and he showed significant improvement. Weight gain was observed throughout hospitalization, but all blood and urine test results showed no metabolic or hematological abnormalities. The patient was discharged for outpatient treatment on clozapine (125 mg morning and 325 mg evening) along with divalproex sodium and metoprolol. Six days post-discharge, the patient died. A medical autopsy later ruled that the death was due to DKA without any evidence of contributory injuries or natural disease. Results and Conclusion Significant increase in body mass index from 28.7 to 33.5 was observed during hospitalization. The blood glucose level, measured after his death, was found to be 500 mg/dL. Altered metabolism due to clozapine can lead to dyslipidemia-mediated-pancreatic-beta-cell damage, decreased insulin secretion as well as insulin resistance. In DKA, low levels of insulin lead to an increased release of free fatty acids from adipose tissue. Acetyl coenzyme A (CoA), derived from the breakdown of free fatty acids, is metabolized by the Kreb's cycle. In hepatocytes, excess acetyl-CoA is converted into ketone bodies (acetoacetate and β-hydroxybutyrate) and released into circulation. Ketone bodies have a low p Ka value and their high serum concentrations lead to DKA. In this patient, DKA was most probably clozapine induced and had fatal consequences. Thus, recognizing potential risk factors, providing patient education, and increasing monitoring of patients on clozapine and other atypical antipsychotics are critical to prevent the life-threatening effects of DKA.

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