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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sequential determinations of glucose outflow and inflow, and rates of gluconeogenesis from alanine, before, during and after insulin-induced hypoglycemia were obtained in relation to alterations in circulating epinephrine, norepinephrine, glucagon, cortisol, and growth hormone in six normal subjects. Insulin decreased the mean (+/-SEM) plasma glucose from 89+/-3 to 39+/-2 mg/dl 25 min after injection, but this decline ceased despite serum insulin levels of 153+/-22 mul/ml. Before insulin, glucose inflow and outflow were constant averaging 125.3+/-7.1 mg/kg per h. 15 min after insulin, mean glucose outflow increased threefold, but then decreased at 25 min, reaching a rate 15% less than the preinsulin rate. Glucose inflow decreased 80% 15 min after insulin, but increased at 25 min, reaching a maximum of twice the basal rate. Gluconeogenesis from alanine decreased 68% 15 min after insulin, but returned to preinsulin rates at 25 min, and remained constant for the next 25 min, after which it increased linearly. A fourfold increase in mean plasma epinephrine was found 20 min after insulin, with maximal levels 50 times basal. Plasma norepinephrine concentrations first increased significantly at 25 min after insulin, whereas significantly increased levels of cortisol and glucagon occurred at 30 min, and growth hormone at 40 min after insulin. Thus, insulin-induced hypoglycemia in man results from both a decrease in glucose production and an increase in glucose utilization. Accelerated glycogenolysis produced much of the initial, posthypoglycemic increment in glucose production. The contribution of glycogenolysis decreased with time, while that of gluconeogenesis from alanine increased. Of the hormones studied, only the increments in plasma catecholamines preceded or coincided with the measured increase in glucose production after hypoglycemia. It therefore seems probable that adrenergic mechanisms play a major role in the initiation of counter-regulatory responses to insulin-induced hypoglycemia in man.
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PMID:The role of adrenergic mechanisms in the substrate and hormonal response to insulin-induced hypoglycemia in man. 0 91

Methods for quantitation of the major apoproteins of human serum very low density lipoprotein have been developed employing tetramethylurea, which delipidates the lipoprotein and selectively precipitates apolipoprotein B. Six soluble apoproteins are separated by electrophoresis in polyacrylamide gel. One of these is a previously unrecognized species of R-alanine (R4-alanine), more anionic than the R3-alanine polypeptide. Conditions of staining have been found which yield reproducibly linear chromogenic response with native lipoprotein and with each purified apoprotein. Recovery of protein in the seven species measured accounts for over 97% of the total in the very low density lipoprotein of normolipidemic individuals and in most samples from individuals with endogenous hyperlipemia. The mean content of apolipoprotein B in 43 samples from normolipidemic subjects was 36.9(+/-1.2 SEM)% of total protein, The distribution of the major soluble apoproteins as mean (+/-SEM) percentage of the soluble fraction was : R-serine, 5.3+/-o.5; arginine-rich, 20.6+/-1.0; R-glutamic, 10.6+/-0.4; R2-alanine, 28.3+/-0.7; R3-alanine, 26.9+/-0.5; and R4-alanine, 8.0+/-0.5. Distribution of the apoproteins was a function of particle diameter of very low density lipoprotein in fractions separated by gel permeation chromatography and by density gradient ultracentrifugation. In fractions below 700-800 A, apolipoprotein B comprised an increasing percentage of the total protein with decreasing particle diameter. Among the soluble proteins the percentage of the arginine-rich and R-serine polypeptides increased and that of the R-glutamic polypeptide declined progressively with decreasing particle size. Apoprotein distribution was similar in fractions of similar particle size from normolipidemic and hyperlipemic subjects with the exception that all fractions from the hyperlipemic subjects contained more R-serine and some, more arginine rich polypeptide. Even in the absence of chylomicrons, the distribution of soluble apoproteins in particles of diameters greater than 700-800 A was usually similar to that of the smallest particles. This suggests that the largest particles may include products of the partial catabolism of chylomicrons.
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PMID:Apoprotein composition of very low density lipoproteins of human serum. 17 34

Panhypopituitarism may be associated with spontaneous hypoglycemia and marked insulin sensitivity. Five children with both growth hormone (GH) and adrenocorticotrophin (ACTH) insufficiency were studied in three periods: a) on no therapy; b) during cortisone acetate; and c) during GH and cortisone acetate replacement. With total caloric restriction prior to therapy, all patients became hypoglycemic (109 +/- 18 leads to 37 +/- 3.5 mg/dl, mean +/- SEM) and ketonemic (beta-hydroxybutyrate 0.10 +/- 0.02 leads to 3.04 +/- 0.63 mM and acetoacetate 0.05 +/- .01 leads to 0.80 +/- 0.15 mM) within 30 hours. Glutamine and alanine concentrations fell with fasting (511 +/- 13 leads to 293 +/- 26 muM and 394 +/- 58 leads to 137 +/- 12 muM, respectively) but to levels lower than in normal children. However, only alanine was significantly lower (P less than 0.05). With cortisone plus GH therapy, fasting glycemia was improved (73 +/- 6 mg/dl) at 30 hours fasting and was associated with increased alanine and glutamine concentrations (206 +/- 28 muM and 448 +/- 40 muM, respectively) and less ketonemia (beta-hydroxybutyrate 1.13 +/- 0.39 mM). Cortisone therapy alone resulted in intermediate improvement of these values. Only combined therapy resulted in increased lactate and pyruvate concentrations, which fell to normal with fasting. Fasting urinary ammonia excretion was unchanged whereas urea nitrogen excretion decreased significantly with therapy. The responses to alanine infusions following each study period in one patient were normal. The glycemic response to iv glucose was similar during each study period; however, post-prandial and glucose-stimulated insulin responses were increased with cortisone and cortisone plus GH therapy. We suggest that the hypoglycemia observed in hypopituitary patients is a substrate-mediated phenomenon, and that cortisone and growth hormone replacement therapy improve fasting glucose homeostasis, increase circulating alanine and glutamine concentrations, and decrease hepatic gluconeogenesis. These effects may be mediated through an increase in fat catabolism.
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PMID:The role of growth hormone and cortisone on glucose and gluconeogenic substrate regulation in fasted hypopituitary children. 17 83

Adrenal steroid secretion rates and the renin-angiotensin-aldosterone (RAA) system were studied in the normothermic marmot. Adrenal secretion by the anesthetized, laparotomized marmot was (mean +/- SEM); aldosterone 1.2 +/- 0.3 ng/min, deoxycorticosterone 16.7 +/- 11.5 ng/min, corticosterone 15.2 +/- 7.8 ng/min, and cortisol 554 +/- 108 ng/min. Four forcings were investigated that affect feedback control at different sites: adrenocorticotropic hormone (ACTH) and angiotensin II (AII) infusion, sodium (Na) depletion, and Na loading. Plasma aldosterone, cortisol, Na, and potassium (K) concentrations as well as plasma renin activity (PRA) hematocrit (Hct), and in some studies, blood pressure were measured. ACTH infusion increased the plasma concentrations of aldosterone and cortisol. AII infusion increased aldosterone concentration, blood pressure, and Hct. Na depletion increased aldosterone, Hct, and PRA; plasma Na and K were decreased. Aldosterone concentration, Hct, and PRA decreased after salt loading. Normothermic, salt-depleted marmots demonstrated a pronounced fall in blood pressure following infusion of the AII analog, 1-sarcosine-8-alanine AII. The average plasma values for aldosterone, PRA, and cortisol found in 44 control animals were: aldosterone 3.8 +/- 0.3 ng/100 ml, PRA 1.9 +/- 0.2 ng AI-ml-1-h-1, and cortisol 54 +/- 4 ng/ml. It was concluded that normothermic marmots have a RAA system comparable to other mammalian species.
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PMID:Renin-angiotensin-aldosterone system of the normothermic marmot. 19 79

The effect of furosemide on plasma renin, vasopressin (AVP), and aldosterone concentrations was studied in 10 control and 6 nephrectomized lambs during the 1st 2 wk of life. In a separate study in 10 newborn lambs, 1-sarcosine-8-alanine-angiotensin II (saralasin acetate, 5 mug/kg per min) was infused alone for 40 min, after which furosemide 2 mg/kg i.v. was injected in association with continuing saralasin acetate infusion. Plasma renin activity increased from a mean (+/-SEM) of 21.3+/-3.4 ng/ml per h in the 10 control lambs to 39.4+/-8.2 ng/ml per h at 8 min (P < 0.001) and remained high through 120 min after furosemide. Plasma AVP and aldosterone concentrations increased from respective mean values of 2.1+/-0.4 muU/ml and 12.8+/-2.5 ng/dl to 9.8+/-2.0 muU/ml (P < 0.01) and 23.0+/-7.7 ng/dl (P < 0.05) at 35 min and 13.8+/-2.1 muU/ml and 23.0+/-4.4 ng/dl at 65 min after furosemide (each P < 0.01). There was an insignificant AVP response in the 10 lambs treated with angiotensin inhibitor: from a mean base line of 4.7+/-0.9 to 8.3+/-2.0 muU/ml at 35 min, and 7.4+/-2.0 muU/ml at 65 min after furosemide. There was no increase in AVP in the anephric lambs. The mean increment AVP response from base line in the newborn lambs without saralasin, Delta 10.8+/-2.0 muU/ml, was greater than in the lambs with saralasin, Delta4.0+/-1.9 (P < 0.05), and greater than in the anephric lambs, Delta3.3+/-2.1 muU/ml (P < 0.05). The mean blood pressure fell 6 mm Hg in the 10 control lambs (P < 0.05), 7 mm Hg in the anephric lambs (P < 0.05), and 16 mm Hg in the lambs treated with angiotensin inhibitor (P < 0.05) by 35 min after furosemide. However, the changes in plasma AVP were not related to the fall in blood pressure. These data support the view that the observed AVP response to furosemide in the newborn lamb was mediated through the renin-angiotensin system.
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PMID:Endogenous angiotensin stimulation of vasopressin in the newborn lamb. 42 54

Turnover rates of 10 amino acids were determined in four normal subjects and 18 burned patients (mean burn size, 41% of total body surface) by measuring leg blood flow by venous occlusion plethysmography and arterial (A) and femoral venous (FV) amino acid concentrations. Patient arterial plasma amino acid concentrations generally were low or normal, although phenylalanine was elevated. Only alanine demonstrated significant A-FV concentration difference (-9 +/- 2 mumole/100 ml in patients vs -5 +/- 1in controls, mean +/- SEM). Leg blood flow was 6.26 +/- 0.57 ml/100 ml of leg volume . min in the patients and 2.62 +/- 0.57 in controls. While the net peripheral release of the 10 amino acids was accelerated following injury, only alanine release was consistently greater in the patients (0.27 plus or minus 0.05 mumole/100 ml in leg volume . min) as compared with that of controls (0.08 +/- 0.02). The increased alanine release from legs of patients generally was related to the extent of total body surface injury and oxygen consumption of the patient, but was unrelated to size of limb burn or leg blood flow. The accelerated rate of alanine release from limbs of burn patients relates to the generalized catabolic effects of injury rather than to local inflammatory or metabolic events which may occur in the injured extremity.
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PMID:Increased peripheral amino acid release following burn injury. 43 18

Glucogon immunoreactivity (IRG) was measured in plasma of duodenopancreatectomized subjects with a nonspecific (K-4023) and a specific (30-K) glucagon antiserum. After an overnight fast, plasma IRG (K-4023) was significantly (P < 0.05) higher in the subjects without pancreas, averaging 782+/-79 (SEM) pgeq/ml, than in the controls (482+/-80 pgeq/ml). IRG (30-K) of 162+/-68 pg/ml did not change during an infusion of arginine (450 mg/kg per 40 min). Insulin deprivation during 3 d in one patient did not restore the IRG response to arginine as reported in depancreatized dogs.Bio-Gel P-30 column chromatography revealed that virtually all IRG (30-K) measured in whole plasma was of different molecular weight than glucagon, and primarily of a mol wt >/= 40,000. Intravenous arginine did not significantly alter the chromatographic pattern of these plasmas. Thus, as postulated by others, duodeno-pancreatectomized humans have virtually no circulating 3,500-dalton glucagon. Hence, the presence of 3,500-dalton glucagon in plasma is not a condition for the diabetic state. It might, nevertheless, when present in normal or excessive amounts, worsen the metabolic state of diabetic patients. Among 14 amino acids measured in plasma of these patients, the concentrations of alanine, serine, ornithine, and arginine were significantly (P < 0.05) elevated to approximately twice that of normal: alanine and serine are both substrates for gluconeogenesis, whereas ornithine and arginine are involved in the formation of urea, the second product of hepatic gluconeogenesis. As the concentrations of branched chain amino acids were not grossly altered, it is hypothesized that this amino acid pattern is a consequence of glucagon deficiency rather than secondary to the diabetic state of these patients.
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PMID:Glucagon immunoreactivities and amino acid profile in plasma of duodenopancreatectomized patients. 44 30

We tested the hypothesis that human growth hormone (hGH) secretion during exercise is related to anaerobic metabolism, and therefore blood lactic acid (LA). Ten males (20 to 30 years) were observed during 40 min of continuous cycle ergometer exercise (CE, 45% of the minimum load which elicited VO2max), and during 20 bouts of intermittent exercise (IE, 1 min on/off at 2x the CE work rate). Continuous and intermittent exercises were used as these are known to result in different LA responses. Resting hGH was 1 to 2 ng/ml. After a lag period, hGH was significantly elevated by 15 min of exercise and thereafter rose continuously in both IE and CE. During IE hGH tended to be higher (12.1 +/- 1.4) than during CE (9.7 +/- 1.6 ng/ml, X +/- SEM), but the difference was not significant. In both exercise conditions free fatty acids demonstrated an initial fall and then a continuous secondary rise with higher peak values during CE (0.52 +/- .06) THAN DURING IE (0.39 +/- .05 mEq/l). Pyruvate (PY) and lactate rose initially during CE, but then declined before reaching steady levels. During IE, LA and PY increased continuously reaching values 3x greater than during CE. Alanine rose progressively during CE and IE, but was significantly higher during IE (442.2 +/- 29.3 vs. 367.9 +/- 30.9 muM). Glucose also tended to be higher during IE (4.67 +/- 0.32) than during CE (4.25 +/- 0.28 mM). Considering CE and IE either together or separately, no physiologically significant correlation was found between hGH and metabolite concentrations, rectal T, or O2 deficit. The results are interpreted to mean that hGH response to work is not directly related to "anaerobiosis".
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PMID:Growth hormone response to continuous and intermittent exercise. 52 44

Renal tubular reabsorption of 3H and 14C labelled L-proline was measured in vivo et situ by continuous microperfusion of single proximal tubules of the rat. The reabsorption is shown to be saturable. Passive diffusion plays a relatively small role in the reabsorption. A maximum possible permeability coefficient of 25 micrometers 2.s-1 for proline was calculated. Two transport systems were found, one with a small affinity and a high capacity, the other with a very high affinity and a small capacity. The following values were estimated. Jmax 1 = 2.6 +/- 0.28 (SEM) nmol.m-1.S-1 Km1 = 11.8 +/- 1.7 (SEM) mmol.1-1 Jmax 2 = 9.6 +/- 1.92 (SEM) pmol.m-1.s-1 Km2 = 29.3 +/- 7.8 (SEM) mumol.1-1. Whereas the first system reabsorbs the bulk of the filtered load, the activity of the second system explains the extremely small amount of proline found in the final urine. Diisopropylphosphorofluoridate--a specific inhibitor of dipeptidyl peptidase IV--decreases the reabsorption of L-proline and L-alanine but has no influence on the reabsorption of the basic amino acid L-arginine and the acidic amino acid L-glutamic acid. This result correlates with a recent speculation that dipeptidyl peptidase IV is involved in proline and alanine reabosrption.
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PMID:Kinetics of L-proline reabsorption in rat kidney studied by continuous microperfusion. 57 61

Hemoglobin (Hb) Alc is a minor component of Hb found in normal individuals but elevated two or threefold in patients with diabetes mellitus. Limited studies have suggested that the level of Hb Alc is proportional to the integrated concentration of glucose over time. Thus it could serve as an index of hyperglycemia. Its measurement may enable a more objective approach to assessing whether or not the control of hyperglycemia can be correlated with the severity of complications of diabetes. Large scale clinicab studies of Hb Alc have not been undertaken for lack of a rapid assay system. This article describes a method of high pressure liquid chromatography (HPLC) which enables the isolation of Hb Alc in 27 min using only 12 microgram of Hb (100 microliter of blood) and a second method for the isolation of total fast Hb components (also elevated in diabetes) in 11 min. Using the first method, a total of 36 assays were performed on the blood of a single normal volunteer over a one month period. the mean level of Hb Alc was 4.95 +/- 0.12% (SD) +/- 0.02% (SEM), while the coefficient of variation (C.V.) was 2.4%. The mean Hb Alc & b level was 1.65 +/- 0.06% +/- 0.01% (C.V. = 3.6%). Values for Hb Alc in 10 normal individuals were 5.06 (mean) +/- 0.32% (SD) +/- 0.01% (SEM). Hb Alc values in 15 patients with diabetes mellitus ranged from 6.8 to 20.0%. The second method was designed to assay Hb Ala, Hb Alb, and Hb Alc as a single peak and yielded results identical to the sum of these components as determined by the first method ( r = 0.98; p less than 0.001).
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PMID:A rapid method for the determination of glycosylated hemoglobins using high pressure liquid chromatography. 62 53


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