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Biomedical subjects

B E Terry

Publications and source records attributed to B E Terry.

At least 37 records · Page 2Linked to original sources
PubMed1987

Comparative effects of forskolin and isoproterenol on the cyclic AMP content of human adipocytes.

Alterations in adipocyte cyclic AMP concentrations in response to 100 microM forskolin and 10 microM isoproterenol over a 4 hour period were found to be similar; with each agent, a peak response was noted within 30 minutes. In general, the greater the magnitude of peak response, the more rapid the decline of cyclic AMP concentration during the ensuing 3 1/2 hours. Alpha-2 adrenergic activation, achieved with 10 microM clonidine or 10 microM epinephrine, substantially reduced the cyclic AMP concentrations in cells stimulated by 100 microM forskolin or 10 microM isoproterenol. Isoproterenol-stimulated cells appeared to be more sensitive to alpha adrenergic inhibition than did forskolin-stimulated cells. Cells preincubated for 3 hours with 100 microM forskolin were markedly less responsive to a second exposure to the diterpine. Cells exposed to forskolin for 3 hours also had a reduced response when incubated with isoproterenol; thus, desensitization to forskolin appears to be heterologous. Forskolin desensitization did not appear to be dependent on cellular ATP depletion since cells mildly stimulated during preincubation were as severely desensitized as those adipocytes strongly stimulated. Maximum desensitization required a preincubation time of 1-2 hours with either isoproterenol or forskolin.

Adipose Tissue↗
PubMed1987

Morbid obesity: cardiac evaluation and function.

The pathophysiology of heart failure in morbid obesity differs from that found in other types of cardiac disease. This article attempts to clarify the myocardial and hemodynamic derangements in morbidly obese subjects. A diagrammatic schema is used to demonstrate the relationship between abnormal function and signs and symptoms of cardiac disease. Noninvasive methods show promise in documenting the effect of enforced weight loss on cardiac function.

Heart Failure↗
PubMed1985

Effect of weight loss on cardiac chamber size, wall thickness and left ventricular function in morbid obesity.

To determine cardiac chamber size, wall thickness and left ventricular (LV) systolic function in morbidly obese patients, M-mode and cross-sectional echocardiography was performed in 62 patients whose body weight was greater than or equal to twice their ideal weight but who were free from underlying organic heart disease and systemic hypertension. The initial clinical protocol consisted of a medical history, physical examination, electrocardiogram at rest, chest x-ray and echocardiogram. Thereafter, each patient underwent gastric restriction. Thirty-four patients returned for follow-up echocardiography 4.3 +/- 0.3 months after substantial weight loss was achieved. For the whole group (n = 62) and LV internal dimension in diastole was enlarged in 24 (39%), the right ventricular internal dimension was enlarged in 20 (32%), the left atrial dimension was enlarged in 25 (40%) and the ventricular septal and LV posterior wall thickness was increased in 35 (56%). In the 34 patients who returned for follow-up, mean body weight decreased significantly, from 135 +/- 8 to 79 +/- 6 kg (73 +/- 4% of the amount over ideal body weight). In the subgroup with low preoperative LV fractional shortening (n = 13), mean LV fractional shortening increased from 22 +/- 2% to 31 +/- 2% (p less than 0.01). This was accompanied by a significant decrease in the mean LV internal dimension in diastole and mean blood pressure. The results indicate that cardiac chamber enlargement, LV hypertrophy and LV systolic dysfunction occur frequently in morbidly obese patients and that LV systolic dysfunction in such persons may improve following substantial weight loss.

Adult↗
PubMed1983

The creation of a surgical endoscopy training program--is there sufficient clinical material?

The American Board of Surgery now requires surgical training programs to provide instruction in gastrointestinal endoscopy. In order to demonstrate that an independent Surgical Endoscopy Service could generate sufficient patient volume for an endoscopy training program, we reviewed our experience before and after the organization of such a service. In the year before formation of the Surgical Endoscopy Service (1981), surgical endoscopists performed 134 upper gastrointestinal (UGI) endoscopies and 25 colonoscopies for a total of 159 procedures. This represented 17% of the total institutional endoscopies performed. Further analysis indicated that 30.5% of UGI endoscopies and 24% of colonoscopies were performed on patients referred from surgical services. During the first year of the Surgical Endoscopy Service (1982), we performed 322 UGI endoscopies and 102 colonoscopies for a total of 424 procedures. This represented an increase to 36.5% of the total institutional endoscopies. During this time 41% of the UGI endoscopies and 33% of the colonoscopies were performed on patients referred from surgical services. Thus, with the formation of a Surgical Endoscopy Service we were able to dramatically increase our procedure volume and to provide effective gastrointestinal endoscopic training for our residency program. This confirmed our premise that in a typical university training program there is sufficient clinical material to provide training in surgical endoscopy.

Academic Medical Centers↗
PubMed1982

Alpha-2 adrenergic activation inhibits forskolin-stimulated adenylate cyclase activity and lipolysis in human adipocytes.

Forskolin at 10 muM caused a 100-fold increase in the intracellular concentration of cyclic AMP and a 6-fold increase in glycerol release in the human adipocyte. These responses are comparable to those prompted by 10 muM isoproterenol. The effects of forskolin on cyclic AMP and lipolysis were dose-dependent. Alpha-2 adrenergic activation, achieved with 10 muM epinephrine and 30 muM propranolol, significantly inhibited forskolin-stimulated cyclic AMP accumulation and glycerol release, shifting the dose-response curves to the right. Forskolin at 10 muM caused a 4.5-fold increase in the adenylate cyclase activity of human adipocyte membranes. When either isoproterenol or epinephrine (0.1 mM) was combined with forskolin, the magnitude of response was substantially greater than the sum of responses achieved by each agent incubated alone.

Adenylyl Cyclases↗
PubMed1982

Studies on desensitization of adrenergic receptors of human adipocytes.

The studies described here were undertaken to determine whether or not desensitization of human adipocyte beta and alpha-2 adrenergic receptors could be demonstrated. Cells, isolated from peritoneal adipose tissue obtained from patients undergoing elective abdominal surgery, were preincubated for 3 hr in buffer alone or in the presence of isoproterenol, 10-5M. Cells in both sets of flasks were then washed and exposed to isoproterenol for 1/2 hr; cyclic AMP was then measured as an end point of beta receptor activation. Cells which had had no prior exposure to isoproterenol responded significantly greater to isoproterenol than did cells that had had prior exposure to the catecholamine, The beta receptor characteristics of cells undergoing beta desensitization were assessed using [3H] dihydroalprenolol. Compared to control cells, adipocytes exposed to isoproterenol had a reduction in Bmax while KD values were the same. Thus desensitization of beta adrenergic receptors of human adipocytes occurs and is associated with down regulation in the number of beta receptors. In comparable studies, preincubation with epinephrine 10-5M did not affect the response of cells to a subsequent exposure to this catecholamine. In alpha-2 receptor binding assays, there was a decreased number of [3H]p-aminoclonidine binding sites, but the level of [3H]yohimbine binding was not altered following the incubation with epinephrine. Thus, desensitization of alpha-2 receptors was not demonstrated.

Adipose Tissue↗
PubMed1981

Pharmacological characterizations of adrenergic receptors in human adipocytes.

Three types of adrenergic receptors, beta, alpha-1, and alpha-2, were identified in human adipocytes, isolated from properitoneal adipose tissue, using both the binding of radioactive ligands and the effects of adrenergic agents on receptor-specific biochemical responses. Adrenergic binding studies showed the following results: [(3)H]dihydroalprenolol binding (beta adrenergic) B(max) 280 fmol/mg protein, K(D) 0.38 nM; [(3)H]para-aminoclonidine binding (alpha-2 adrenergic) B(max) 166 fmol/mg protein, K(D) 0.49 nM; [(3)H]WB 4101 binding (alpha-1 adrenergic) B(max) 303 fmol/mg protein, K(D) 0.86 nM. In adipocytes from subcutaneous adipose tissue, [(3)H]dihydroergocryptine binding indicated the presence of alpha-2 but not alpha-1 receptors. Beta and alpha-2 adrenergic receptors appeared to be positively and negatively coupled to adenylate cyclase, respectively. Cells or cell membranes were incubated with epinephrine (10 muM) alone and in combination with the antagonists yohimbine (alpha-2) and prazosin (alpha-1). Epinephrine alone prompted a modest increase in adenylate cyclase activity, cyclic AMP, and glycerol release, an index of lipolysis. Yohimbine (0.1 muM) greatly enhanced these actions whereas prazosin was without effect. The beta agonist, isoproterenol, stimulated glycerol release, whereas the alpha-2 agonist, clonidine, inhibited lipolysis and cyclic AMP accumulation. To assess further alpha-1 receptors, cells were incubated with [(32)P]phosphate and epinephrine (10 muM) alone and in combination with prazosin and yohimbine. Epinephrine alone caused a three- to fourfold increase in (32)P incorporation into phosphatidylinositol. Prazosin (0.1 muM) blocked this action whereas yohimbine (0.1 muM) was without effect. Thus, in a homogeneous cell preparation, the human adipocyte appears to have three different adrenergic receptors, each of which is coupled to a distinct biochemical response.

Adenylyl Cyclases↗
PubMed1979

Insulin inhibition of lipolysis of human adipocytes: the role of cyclic adenosine monophosphate.

To gain information on the manner in which insulin suppresses lipolysis in man, isolated adipocytes, prepared from subcutaneous adipose tissue, were incubated with insulin (100 microunits/ml) alone and in combination with isoproterenol (10(-7) M or 10(-8) M). Cyclic AMP concentration was measured at 60 min; glycerol release, used as an index of lipolysis, was determined at 45 and 75 min. Insulin consistently reduced both basal and stimulated cyclic AMP and glycerol release: the degree of suppression of each was comparable. In subsequent experiments, the ability of insulin to suppress glycerol release stimulated by isoproterenol, theophylline, and dibutyryl cyclic AMP (dbcAMP), respectively, was compared. Insulin substantially reduced the raised levels of cyclic AMP and glycerol release prompted by isoproterenol and theophylline, but it had little effect on increases caused by dbcAMP. These findings support the view that reduction in cyclic AMP is an important component in the regulation of fat mobilization by insulin.

Adipose Tissue↗
PubMed1979

The effect of fasting on the adrenergic receptor activity of human adipocytes.

To assess the influence of fasting of the alpha- and beta-adrenergic receptor activities of human adipocytes, subcutaneous adipose tissue was obtained from normal obese subjects in the fed state and after 3 days of fasting. Isolated cells prepared from the adipose tissue were incubated with epinephrine, 10(-6)M, and in the presence of the alpha-blocker phentolamine, 10(-5)M, and the beta-blocker propranolol, 10(-5)M, respectively; intracellular cyclic AMP levels and glycerol released into the buffer were measured. Consistent with past observations, epinephrine stimulated cyclic AMP and glycerol release when incubated with cells from fed subjects. Phentolamine enhanced this action and propranolol reduced it below the basal level. In contrast, epinephrine suppressed cyclic AMP and lipolysis when incubated with adipocytes from fasted individuals. This reversal in the effect of epinephrine on adipocy.se in alpha-activity. Additional studies suggest that this change in alpha- and beta-adrenergic receptor balance occurred after 1 day of fast and was not significantly exaggerated when fast was prolonged to 8 days. These findings are consistent with the view that in the fasting state the sympathetic nervous system and circulating catecholamines act to conserve adipose tissue triglyceride.

Adipose Tissue↗
PubMed1978

The role of free fatty acids in the regulation of lipolysis by human adipose tissue cells.

The effect of added fatty acid on lipolysis and cyclic AMP concentration of human adipose tissue cells was studied. The addition of sodium oleate decreased the lipolytic response of adipocytes to 10(-7) M isoproterenol. Inhibition was detectable with the lowest quantity of oleate added, 0.2 mM, and was progressively greater with increasing quantities of added fatty acid. Palmitic and linoleic acids were as effective as oleic acid in suppressing isoproterenol-stimulated lipolysis. Suppression of cyclic AMP formation was detectable within one minute after the addition of oleate. Cyclic AMP formation, suppressed by accumulated fatty acids, could not be stimulated by the addition of fresh isoproterenol. However, after the accumulated fatty acids were removed by buffer change, cyclic AMP formation was stimulated by fresh isoproterenol. These findings are consistent with the view that fatty acids are physiologically significant regulators of lipolysis.

Adipose Tissue↗
PubMed1977

In-vitro observations on isolated adipose tissue cells from hyperobese subjects.

Isolated adipose tissue cells were prepared from subcutaneous samples obtained from nine morbidly obese subjects weighing from 187 to 306% of ideal body weight. The responsiveness of these adipocytes to a number of test substances was determined by measuring cellular cyclic AMP concentration at one-half hour and glycerol release at four hours. Theophylline (10(-3) M) and epinephrine (10(-5) M) stimulated lipolysis; theophylline stimulated an increase in cyclic AMP, while epinephrine failed to prompt a significant change in the nucleotide. Neither the alpha blocker, phentolamine (10(-5) M), nor the beta blocker, propranolol (3 X 10(-5) M), affected lipolysis or cyclic AMP; when these agents were incubated in combination with epinephrine, changes occurred indicative of the presence of both alpha and beta adrenergic receptor sites. Insulin significantly reduced both basal and stimulated lipolysis but failed to affect cyclic AMP. With minor exceptions, adipocytes from hyperobese subjects behaved similarly to cells from unselected donors; at the concentration used, there was no evidence of resistance to insulin.

Adipose Tissue↗
PubMed1976

Some nutrient interrelations during total intravenous alimentation in adult man--a review.

Selected aspects of total parenteral nutrition in man are reviewed with emphasis on carbohydrate, lipid, and hormonal interactions. In an experiment to test for the essentiality of a specific amino acid, a normal adult man received all major and minor nutrients, except lipids, by intravenous alimentation for 48 days. A chemical deficiency of essential fatty acids without clinical symptoms was promptly observed in four plasma lipid fractions and the phospholipid fraction of erythrocytes. With the glucose providing 2,600 kcal/day, blood glucose remained normal, but a hypertriglyceridemia was observed. Plasma insulin rose and cortisol fell. To meet the essential fatty acid and energy requirements of man, critical experiments are needed to define the safe utilization of lipid emulsions during prolonged intravenous nutrition.

Adult↗