scholarly journals Albumin Knockout Mice Exhibit Reduced Plasma Free Fatty Acids but No Impairment in Whole Body Fat Oxidation

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 534-534
Author(s):  
Afsoun Abdollahi ◽  
Brianana N Dowden ◽  
Gregory C Henderson
Keyword(s):  
Fatty Acids ◽  
Serum Albumin ◽  
Free Fatty Acids ◽  
Body Fat ◽  
Knockout Mice ◽  
Substrate Oxidation ◽  
Whole Body ◽  
Wild Type ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa

Abstract Objectives To improve understanding of the control of lipid metabolism, we aimed to determine whether lack of serum albumin decreases plasma free fatty acids (FFA), hepatic triacylglycerol (TAG), and whole body substrate oxidation in albumin knockout mice compared to wild type mice. Methods Male and female homozygous albumin knockout mice and C57BL/6J wild type controls, each on the 5k52 diet which contains a moderate fat content, were studied at 6–8 weeks of age. Body composition was tested by magnetic resonance. Substrate oxidation was measured by indirect calorimetry over 24 hours in metabolic cages. Plasma and tissues were collected after a 5-hour fast. Plasma FFA was measured by liquid chromatography/mass spectrometry (LC/MS). Hepatic TAG was measured by a colorimetric kit. Results In albumin knockout mice compared to the wild type mice, plasma FFA (P < 0.0001) and hepatic TAG content (P < 0.0001) were each reduced, while body fat percentage was increased (P < 0.01). In addition, female versus male showed higher hepatic TAG levels (P < 0.01). These results indicate that the lack of serum albumin decreases plasma FFA and hepatic TAG accumulation. However, the average 24-hour oxygen consumption, metabolic rate, and respiratory quotient (RQ) were not altered in albumin knockout mice, indicating that total fuel oxidation and relative contribution of lipid to whole body metabolism was not significantly unaltered. Conclusions We propose that lack of albumin reduces plasma FFA which diminishes hepatic TAG content through changes in the lipid supply to the liver. The results indicate that tissue lipid accumulation can be altered by targeting albumin without substantially disrupting whole body substrate oxidation, suggesting that metabolic control of FFA trafficking toward sites of ectopic lipid deposition and toward oxidation can be regulated independently of one another. Funding Sources McKinley Educational Initiative and the Purdue University College of Health and Human Sciences

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.

Factors Affecting Plasma Free Fatty Acids Rise during Hemodialysis

1988 ◽  
Vol 11 (2) ◽  
pp. 95-98 ◽  
Author(s):  
G. Mingardi ◽  
E. Branca ◽  
M. Cini ◽  
A.M. Codegoni ◽  
G. Mecca ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasma Lipids ◽  
Unknown Mechanism ◽  
Factors Affecting ◽  
Plasma Free Fatty Acids ◽  
Plasma Triglycerides ◽  
Plasma Ffa ◽  
Acute Changes

We studied the mechanisms responsible for causing acute changes in plasma lipids during hemodialysis. Dialysis decreased plasma triglycerides to the same extent as when heparin was given without dialysis. Cholesterol increased in proportion to hemoconcentration. Plasma free fatty acids (FFA) levels were also increased, but more so than with heparin alone. Glucose and acetate did not play a role, nor did carnitine loss, and hemofiltration elicited similar effects. The rise in plasma FFA is therefore likely to be caused by other as yet unknown mechanism.

Plasma free fatty acids in exercise

1964 ◽  
Vol 19 (3) ◽  
pp. 489-492 ◽  
Author(s):  
K. Rodahl ◽  
H. I. Miller ◽  
B. Issekutz
Keyword(s):  
Fatty Acids ◽  
Lipid Metabolism ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Blood Sugar ◽  
Blood Lactate ◽  
Marked Change ◽  
Apparent Discrepancy ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa

The effects of exercise of different intensity and duration on plasma free fatty acids (FFA), blood glucose, and lactate were investigated in eight healthy young men. In heavy 10-min work the blood lactate rose rapidly and the FFA decreased. Blood sugar showed no marked change. Intermittent work caused a slight increase in blood lactate and no change in blood glucose. The FFA remained essentially unchanged but increased in three out of four subjects during recovery. In moderate 1-hr work the FFA remained essentially unchanged, but increased markedly during recovery when blood lactate had returned to resting levels. In prolonged exhausting work in fasting subjects, the blood lactate remained almost unchanged, while the FFA rose steadily and the blood sugar dropped. In nonfasting subjects the FFA also rose, but the ingestion of lunch caused, in all cases, a striking drop in the FFA, associated with a rise in blood sugar. Combined hormonal effects (insulin and norepinephrine) brought into play during exercise of different intensity and duration may well explain the apparent discrepancy in the results of different investigators concerning the effect of exercise on plasma FFA. work and FFA; FFA at different workloads; lipid metabolism in work Submitted on November 6, 1963

Abstract 024: Plasma Free Fatty Acids and Risk of Dementia: The Cardiovascular Health Study

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Majken K Jensen ◽  
Petra Buzkova ◽  
Annette L Fitzpatrick ◽  
W. T. Longstreth ◽  
Lewis H Kuller ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cognitive Decline ◽  
Free Fatty Acids ◽  
Cardiovascular Health ◽  
Apoe Genotype ◽  
Health Study ◽  
Cardiovascular Health Study ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa ◽  
Plasma Ffas

Background: Plasma free fatty acids (FFAs) are a byproduct of lipolysis largely derived from adipose tissue. High plasma FFA levels have toxic effects on a variety of organs central to cardiometabolic disease. Whether FFAs associates with cognitive decline or dementia remains unknown. Objective: To assess the association of plasma FFAs with risk of cognitive decline and dementia. Methods: Plasma FFAs were measured in participant samples from the 1992-1993 study visit of the Cardiovascular Health Study (CHS) (mean age 74 yrs; 59% female; 14% African American [AA]; 24% APOE4 carriers). A total of 3,242 non-demented participants were followed with adjudication for dementia through 1998-1999 (n=456 cases). In addition, cognitive decline was assessed annually among all CHS participants using the 100-point modified Mini-Mental State examination (3MSE; n=4,417) and the Digital Symbol Substitution Test (DSST; n=4,254). Results: Higher plasma FFAs levels were positively associated with risk of dementia (Figure: Log-rank p-value=0.04). In Cox regression analysis adjusted for demographics, FFAs remained associated with risk of dementia (HR per SD [0.20 mEq/L] =1.10; 95% CI, 1.00-1.22). In fully adjusted models that included lifestyle factors, medical history, C-reactive protein, LDL-C, HDL-C, and 3MSE at baseline, the hazard ratio per SD was 1.13 (1.01-1.26), with a particularly strong association observed among AA participants (HR=1.49 [1.10-2.01], p interaction=0.08). FFA levels did not differ by APOE genotype, and adjustment for genotype did not influence results. FFA levels from the baseline visit were also associated with a decline in both cognitive assessments over 6 years of follow-up, with significant time x FFA interactions (p=0.04 for 3MSE and p=0.002 for DSST). We observed no interactions with APOE genotype or race for cognitive outcomes. Conclusions: In non-demented older men and women, higher plasma FFA levels are associated with faster cognitive decline and higher risk of dementia over the subsequent years.

THE ROLE OF PLASMA FREE FATTY ACIDS IN THE ELEVATION OF PLASMA CHOLESTEROL AND PHOSPHOLIPIDS PRODUCED BY ADRENALINE

1966 ◽  
Vol 36 (3) ◽  
pp. 301-316 ◽  
Author(s):  
A. M. BARRETT
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasma Cholesterol ◽  
Hormone Secretion ◽  
Oral Glucose ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa ◽  
Adrenocortical Hormone ◽  
Glucose Plasma ◽  
Acute Changes

SUMMARY The effects of adrenaline, noradrenaline, corticotrophin (ACTH), cortisol and corticosterone on the levels of blood lipids have been studied in dogs and rats. Blood glucose, plasma free fatty acids (FFA) and corticosteroids were determined 4 hr. after injection. Plasma cholesterol, phospholipids and triglycerides were determined 24 hr. after the last of three daily treatments. In some experiments an oral glucose load was given at the same time as the hormones. In dogs plasma FFA were increased by adrenaline and noradrenaline, decreased by ACTH plus glucose and not affected by ACTH alone. Gradual rises in the lipoprotein levels of dogs were produced by any of the hormones given and followed acute rises in corticosteroid concentration regardless of the acute changes in plasma FFA. In rats plasma FFA were increased by adrenaline and ACTH, decreased by glucose and not affected by ACTH plus glucose. It was not possible to produce rises in lipoprotein by administering adrenaline or ACTH to rats. Exogenous corticosteroids produced increases in the cholesterol and phospholipid levels. The effects of corticosterone were potentiated by oral glucose but cortisol produced a full effect without extra glucose. The FFA responses to subcutaneous adrenaline in rats were reduced by adrenalectomy, but the increases in plasma FFA produced by intravenous infusion of adrenaline or ACTH were similar in adrenalectomized and intact rats. It was concluded that changes in lipoproteins are not causally related to increased mobilization of FFA but are dependent on increased adrenocortical hormone secretion in the presence of excess carbohydrate.

A fat-mobilizing substance in chicken urine

1969 ◽  
Vol 47 (5) ◽  
pp. 435-443 ◽  
Author(s):  
I. Nir ◽  
Mildred K. Dimick ◽  
S. Lepkovsky
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Food Intake ◽  
Free Fatty Acids ◽  
Plasma Cholesterol ◽  
Lipid Phosphorus ◽  
Male And Female ◽  
Plasma Free Fatty Acids ◽  
Plasma Triglycerides ◽  
Plasma Ffa

A fat-mobilizing substance (FMS) was extracted from the urine of fasting male and female chickens. Injection into chickens caused transient decreases in food intake and transient increases in plasma free fatty acids (FFA). These effects were accompanied by persisting decreases in plasma triglycerides. FMS also caused persistent decreases in plasma cholesterol and lipid phosphorus. Slight elevations of blood glucose occurred, but they were not statistically significant. FMS obtained from the urine of fed chickens by the same technique as that used with fasting chickens varied in its activity; at times it was similar to the FMS obtained from fasting chickens and at other times had little effect on plasma FFA and food intake. FMS elicited smaller increases in plasma FFA in laying hens than it did in males, possibly as a result of higher pre-injection levels in the hens. In contrast to findings in mammals, FMS was obtained from the urine of hypophysectomized chickens. Differences in response to FMS among mice, rats, and chickens are discussed.

scholarly journals Free fatty acids, glicentin and glucose-dependent insulinotropic polypeptide as potential major determinants of fasting substrate oxidation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julia Hummel ◽  
Louise Fritsche ◽  
Andreas Vosseler ◽  
Corinna Dannecker ◽  
Miriam Hoene ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Body Fat ◽  
Respiratory Quotient ◽  
Substrate Oxidation ◽  
Oral Glucose ◽  
Fasting State ◽  
The Metabolic Syndrome ◽  
Fuel Selection

AbstractThe selection of carbohydrates or fat to generate intracellular energy is thought to be crucial for long-term metabolic health. While most studies assess fuel selection after a metabolic challenge, the determinants of substrate oxidation in the fasted state remain largely unexplored. We therefore assessed the respiratory quotient by indirect calorimetry as a read-out for substrate oxidation following an overnight fast. This cross-sectional analysis consisted of 192 (92 women, 100 men) either lean or obese participants. Following an overnight fast, the respiratory quotient (RQ) was assessed, after which a 5-point 75-g oral glucose tolerance test was performed. Unlike glucose and insulin, fasting free fatty acids (FFA) correlated negatively with fasting RQ (p < 0.0001). Participants with high levels of the ketone body β-hydroxybutyric acid had significantly lower RQ values. Fasting levels of glucose-dependent insulinotropic polypeptide (GIP) and glicentin were positively associated with fasting RQ (all p ≤ 0.03), whereas GLP-1 showed no significant association. Neither BMI, nor total body fat, nor body fat distribution correlated with fasting RQ. No relationship between the RQ and diabetes or the metabolic syndrome could be observed. In the fasting state, FFA concentrations were strongly linked to the preferentially oxidized substrate. Our data did not indicate any relationship between fasting substrate oxidation and metabolic diseases, including obesity, diabetes, and the metabolic syndrome. Since glicentin and GIP are linked to fuel selection in the fasting state, novel therapeutic approaches that target these hormones may have the potential to modulate substrate oxidation.

PPAR-α activation required for decreased glucose uptake and increased susceptibility to injury during ischemia

2005 ◽  
Vol 288 (6) ◽  
pp. H2677-H2683 ◽  
Author(s):  
Marcello Panagia ◽  
Geoffrey F. Gibbons ◽  
George K. Radda ◽  
Kieran Clarke
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Null Mouse ◽  
Elevated Plasma ◽  
Wild Type ◽  
Plasma Free Fatty Acids ◽  
Protein Levels ◽  
Glut 4 ◽  
Metabolic States

The transcription of key metabolic regulatory enzymes in the heart is altered in the diabetic state, yet little is known of the underlying mechanisms. The aim of this study was to investigate the role of peroxisome proliferator-activated receptor-α (PPAR-α) in modulating cardiac insulin-sensitive glucose transporter (GLUT-4) protein levels in altered metabolic states and to determine the functional consequences by assessing cardiac ischemic tolerance. Wild-type and PPAR-α-null mouse hearts were isolated and perfused 6 wk after streptozotocin administration or after 14 mo on a high-fat diet or after a 24-h fast. Myocardial d-[2-3H]glucose uptake was measured during low-flow ischemia, and differences in GLUT-4 protein levels were quantified using Western blotting. In wild-type mice in all three metabolic states, elevated plasma free fatty acids were associated with lower total cardiac GLUT-4 protein levels and decreased glucose uptake during ischemia, resulting in poor postischemic functional recovery. Although PPAR-α-null mice also had elevated plasma free fatty acids, they had neither decreased cardiac GLUT-4 levels nor decreased glucose uptake during ischemia and, consequently, did not have poor recovery during reperfusion. We conclude that elevated plasma free fatty acids are associated with increased injury during ischemia due to decreased cardiac glucose uptake resulting from lower cardiac GLUT-4 protein levels, the levels of GLUT-4 being regulated, probably indirectly, through PPAR-α activation.

Evidence for an Hepatic Anti-Ketogenic Effect of Insulin in Man

1978 ◽  
Vol 55 (5) ◽  
pp. 499-504 ◽  
Author(s):  
R. S. Elkeles ◽  
R. A. Chalmers ◽  
J. Hambley
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Direct Effect ◽  
Normal Subjects ◽  
Oral Glucose ◽  
Plasma Free Fatty Acids ◽  
Sharp Fall ◽  
Plasma Ffa ◽  
Effect Of Glucose

1. Infusion of a triglyceride emulsion (Intralipid) into overnight fasted normal subjects produced a rise in plasma free fatty acids (FFA) and blood ketones. 2. Glucose given orally 60 min after the start of the Intralipid infusion produced a sharp fall in blood ketones without much change in plasma FFA. 3. An infusion of glucagon given together with Intralipid did not alter the reduction in blood ketones produced by oral glucose in normal subjects. 4. Oral glucose given 60 min after the start of the Intralipid infusion in three insulin-requiring diabetic subjects produced no fall in blood ketones. 5. The results suggest that glucose prevents the increase in blood ketones after Intralipid through an increase in insulin secretion rather than through a suppression of glucagon or as a direct effect of glucose. 6. It is most likely that the effect of insulin is to inhibit hepatic ketogenesis.

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