A fat-mobilizing substance in chicken urine

1969 ◽  
Vol 47 (5) ◽  
pp. 435-443 ◽  
Author(s):  
I. Nir ◽  
Mildred K. Dimick ◽  
S. Lepkovsky

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.

1988 ◽  
Vol 11 (2) ◽  
pp. 95-98 ◽  
Author(s):  
G. Mingardi ◽  
E. Branca ◽  
M. Cini ◽  
A.M. Codegoni ◽  
G. Mecca ◽  
...  

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.


1964 ◽  
Vol 19 (3) ◽  
pp. 489-492 ◽  
Author(s):  
K. Rodahl ◽  
H. I. Miller ◽  
B. Issekutz

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


1966 ◽  
Vol 36 (3) ◽  
pp. 301-316 ◽  
Author(s):  
A. M. BARRETT

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.


1963 ◽  
Vol 204 (4) ◽  
pp. 691-695 ◽  
Author(s):  
H. C. Meng ◽  
B. Edgren

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.


1988 ◽  
Vol 255 (4) ◽  
pp. R547-R556 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
L. Benthem

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.


2002 ◽  
Vol 282 (2) ◽  
pp. E402-E411 ◽  
Author(s):  
Chang An Chu ◽  
Stephanie M. Sherck ◽  
Kayano Igawa ◽  
Dana K. Sindelar ◽  
Doss W. Neal ◽  
...  

The aim of this study was to determine the effect of high levels of free fatty acids (FFA) and/or hyperglycemia on hepatic glycogenolysis and gluconeogenesis. Intralipid was infused peripherally in 18-h-fasted conscious dogs maintained on a pancreatic clamp in the presence (FFA + HG) or absence (FFA + EuG) of hyperglycemia. In the control studies, Intralipid was not infused, and euglycemia (EuG) or hyperglycemia (HG) was maintained. Insulin and glucagon were clamped at basal levels in all four groups. The arterial blood glucose level increased by 50% in the HG and FFA + HG groups. It did not change in the EuG and FFA + EuG groups. Arterial plasma FFA increased by ∼140% in the FFA + EuG and FFA + HG groups but did not change significantly either in the EuG or HG groups. Arterial glycerol levels increased by ∼150% in both groups. Overall (3-h) net hepatic glycogenolysis was 196 ± 26 mg/kg in the EuG group. It decreased by 96 ± 20, 82 ± 16, and 177 ± 22 mg/kg in the HG, FFA + EuG, and FFA + HG groups, respectively. Overall (3-h) hepatic gluconeogenic flux was 128 ± 22 mg/kg in the EuG group, but it was suppressed by 30 ± 9 mg/kg in response to hyperglycemia. It was increased by 59 ± 12 and 56 ± 10 mg/kg in the FFA + EuG and FFA + HG groups, respectively. In conclusion, an increase in plasma FFA and glycerol significantly inhibited hepatic glycogenolysis and markedly stimulated hepatic gluconeogenesis.


1971 ◽  
Vol 118 (545) ◽  
pp. 429-436 ◽  
Author(s):  
Werner H. Schimmelbusch ◽  
Peter S. Mueller ◽  
Jack Sheps

Various abnormalities have been demonstrated in schizophrenic patients in response to injected insulin. Thomaset al.(22), Harris (8), Freemanet al.(7), Mayer-Gross (10), and Bracelandet al.(4) have shown a delayed or decreased response of blood glucose to insulin in schizophrenic patients. Meduna and McCulloch (11) observed that those schizophrenic patients who suffered from confusion and clouding of the sensorium particularly displayed a delayed or decreased response to injected insulin as well as a urinary hyperglycaemic factor and decreased tolerance to oral and intravenous glucose. Subsequent studies by Mueller (12, 13) demonstrated a rise or lack of fall in the plasma free fatty acids (FFA) following the administration of insulin intramuscularly or intravenously in chronic schizophrenic patients. Van Sickleet al.(23) confirmed these findings of insulin resistance in chronic schizophrenia and noted that this low FFA response was neither related to an abnormal release of, nor response to, epinephrine.


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