Leonard J. Feinberg

The Role of Catecholamines in the Free Fatty Acid Response to Cigarette Smoking

The role of the adrenal glands and the sympathetic nervous system in the free fatty acid (FFA) rise after smoking was investigated.In 11 subjects who smoked three cigarettes per hour for a 3-hour period, urinary free catecholamine excretion increased 2.5 &mgr;g./hr. (21 per cent) and total catecholamine excretion increased 3.1 &mgr;g./hr. (16 per cent). FFA elevations occurred in all subjects during the smoking period.In three subjects, repeated control determinations of their FFA response to smoking were made and a rise was observed in each instance. Sympathetic ganglionic blockade was then induced with methaphan camphorsulfonate and the smoking tests were repeated. No rise in FFA after smoking occurred following blockade.Eight patients, who had previously undergone bilateral adrenalectomy for the treatment of hypertension, were studied for their FFA response to smoking. In six subjects there was no significant elevation. In two subjects there was a minimal effect.These findings indicate that for cigarette smoking to cause an increase in serum free fatty acids both the adrenal glands and the sympathetic nervous system must be functioning, probably to produce an effective level of circulating catecholamines.

Effect of cigarette smoking and nicotine on serum free fatty acids based on a study in the human subject and the experimental animal.

The effect of cigarette smoking on serum free fatty acids (FFA) was studied in human subjects. After smoking two cigarettes there was an average maximal elevation in FFA of 351 μEq./L. This usually occurred 10 minutes after smoking and, in most instances, there was still some elevation 20 and 40 minutes after smoking. There was essentially no effect on serum cholesterol and triglyceride levels. In subjects who “chain-smoked” six cigarettes, all showed a rise in FFA during a 60-minute period, one showing a three-fold elevation. The effect of intravenous nicotine on serum FFA was studied in dogs. In 13 of 15 observations there was a rise in FFA. The mean maximal elevation of 166 μEq./L. occurred after 10 minutes of nicotine infusion. These effects are probably due to sympathetic and adrenal stimulation by nicotine. This results in a rise in circulating catecholamines which rapidly effect a mobilization of FFA from the fat stores in the body.

Effects of coffee ingestion on oral glucose tolerance curves in normal human subjects

Abstract Oral glucose tolerance tests were performed on 23 normal subjects and then repeated one week later. On one occasion, the test meal consisted of glucose dissolved in water and flavored with lemon juice; on the other occasion, 5 Gm. of instant coffee were also added to the meal. The order of administration of the respective meals was randomized. Serial blood samples were obtained and analyzed for blood glucose concentration, serum free fatty acid levels and the serum immunoreactive insulin values. Paired comparisons of the data were made and the following results were obtained: (1) The subjects ingesting coffee plus glucose had significantly lower blood glucose levels 30 and 60 minutes postprandium than those consuming the glucose solution without coffee. (2) Three hours after ingestion of the test meal, the free fatty acid levels of the subjects receiving coffee with glucose were significantly higher than those receiving glucose without coffee. (3) No statistically significant differences between the two groups were found at any time period for the serum immunoreactive insulin levels. It is possible that coffee ingestion reduced the peak postprandial blood glucose levels by mobilizing a hormone from the gastrointestinal tract such as secretin, pancreozymin, or the newly discovered substance with glucagon-like immunoreactivity described by Unger et al37.

Effect of cigarette smoking on free fatty acids in patients with healed myocardial infarction

Abstract The effect of smoking on serum free fatty acids was studied in 17 patients with healed myocardial infarction. There was an elevation of FFA in all subjects after smoking two cigarettes in a 10 minute period. A mean maximal rise of 858 μEq. L. (65.6 per cent) occurred 10 to 20 minutes after smoking, and usually some elevation persisted for 40 minutes. Noncoronary patients and normal subjects also developed FFA elevations of 320 μEq. L. (27.2 per cent) and 292 μEq. L. (24.6 per cent), respectively. It is suggested that the greater FFA response in myocardial infarction patients is the result of a greater catecholamine release after nicotine stimulation.

Effects of various routes of caffeine administration on oral and intravenous glucose tolerance tests in dogs

Abstract Oral glucose tolerance tests were performed four times on 15 dogs with an interval of at least three days between each test: glucose solution alone formed the test meal; caffeine sodium benzoate was mixed with the glucose solution and fed to the animal; glucose solution was administered orally and caffeine was given intravenously; the glucose solution was given orally and the caffeine was administered intramuscularly. The order of administration of the respective tests was randomized. Blood samples were taken at serial intervals and analyzed for blood glucose and serum immunoreactive insulin levels. Intravenous glucose tolerance tests were also run four times on 11 dogs where the regimen consisted of glucose solution alone, glucose intravenously and caffeine intravenously, glucose I.V. and caffeine orally, and glucose I.V. and caffeine I.M. Serial blood samples were drawn and likewise analyzed for glucose and immunoreactive insulin values. The oral glucose tolerance tests were markedly altered by administration of caffeine. Thirty, 60 and 90 minutes after the ingestion of caffeine blood glucose was significantly lower than the untreated group (p=

Effect of Cold, Adrenocorticotropic and Thyroid Hormones on Urinary Excretion of Pentose in the Rat.

Summary Low temperatures and thyroid administration increased significantly the urinary excretion of pentose in rats. ACTH administration had a preventive effect upon the increased pentosuria due to cold.

Effect of dihydroergotamine on plasma Free Fatty Acids (FFA) in dogs

Abstract Dihydroergotamine, in doses of 0.125 and 0.5 mg/kg, I.V., significantly increased plasma concentrations of FFA in dogs. The maximal effect was reached in 30 minutes; the duration of action exceed 4 hours. Propranolol, 2 mg/kg, I.V., delayed but did not abolish, the effect of dihydroergotamine on the plasma FFA. Adrenalectomy or mecamylamine, 0.5 mg/kg, I.V., had no effect on dihydroergotamine induced elevation of plasma FFA. dogs pretreated with reserpine, dihydroergotamine produced a greater rise in plasma FFA than in control animals. Nicotinic acid, 40 mg/kg, I.V., abolished the effect of dihydroergotamine. It was concluded that the effect of dihydroergotamine on plasma FFA in dogs is not mediated by sympathetic nervous system, release of norepinephrine from the reserpine-sensitive storage sites, or liberation of epinephrine from the adrenal medulla. Dihydroergotamine may stimulate adrenergic receptors of the adipose tissue, or activate lipolytic mechanisms beyond adrenergic receptors. Its action may also be mediated by non-adrenergic endogenous lipolytic substances.

Production of potassium depletion by benzothiadiazine compounds

Abstract Secondary hyperaldosteronism was simulated in seven patients by the administration of desoxycorticosterone acetate (DCA) in doses of 30 mg. per day. In these patients the sodium-retaining properties of this agent appeared to be independent of total exchangeable sodium. The combined administration of hydrochlorothiazide and DCA resulted in a significantly greater kaliuretic effect than that of the sum of the two given separately. Similar results were obtained with other benzothiadiazine compounds. In conditions associated with secondary hyperaldosteronism, i.e., portal cirrhosis with ascites, nephrosis and malignant hypertension, the benzothiadiazine derivatives are likely to produce moderate to severe potassium epletion. Claims that one benzothiadiazine compound causes less potassium depletion than another are meaningless unless endogenous aldosterone secretion is considered.

The effects of clofibrate on the metabolism of C14 labeled tripalmitin in the human subject

Abstract Eight patients were treated for several weeks with chlorophenoxyisobutyrate (CPIB). Serum triglycerides, phospholipids and cholesterol concentrations were determined before and after therapy. In addition, C 14 tripalmitin was administered orally in a test meal to the subjects before and after therapy with CPIB and the radioactivity in the lipid extractable fractions of the blood and in the lipoprotein fractions of the serum (density 1.063, respectively) were measured 2, 4, 6, 8 and 24 hours after the test meal. Significant drops in the serum triglycerides as well as lowered levels of radioactivity in the serum VLDLP were observed in the majority of the cases. No significant lowering of the serum cholesterol or phospholipids were noted.

Effects of varying rates of sodium excretion on Na22 kinetics.

Summary Biological decay curves of Na22 excretion showed good correlation with urinary sodium excretion during alteration of sodium excretion by sodium chloride, DCA and hydrochlorothiazide over periods of 3 to 7 days. During these short intervals, biological decay curves of serum radioactivity and serum specific activity were too variable to allow correlation with urinary sodium excretion. Daily total exchangeable sodium shows a progressive rise and cannot be used to reflect acute changes in sodium balance.