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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth rate, plasma amino acid, and alpha-keto acid concentrations and activities of the branched-chain amino acid degradative enzymes of rats were measured. Effects of ingestion of excessive amounts of branched-chain amino acids on these variables were determined. Excessive intake of a single branched-chain amino acid led rapidly to elevated plasma concentration of both the amino acid administered and its corresponding alpha-keto acid and, if the rats had previously been fed a low protein diet, to an increase in liver branched-chain alpha-keto acid dehydrogenase activity. Only leucine caused, in addition, marked growth and food intake depression and decreased plasma isoleucine, valine, alpha-keto-beta-methylvaleric acid and alpha-keto isovaleric acid concentrations. The growth depression was associated food intake depression and could be moderated by addition of isoleucine and valine to the diet. The decreases in plasma isoleucine, valine, alpha-keto-beta-methylvaleric acid and alpha-keto isovaleric acid were not caused by increased degradation of these metabolites to carbon dioxide as branched-chain amino acid oxidation rates in vivo were unchanged by leucine loading and the degradative enzymes were unchanged in adequately fed rats. The decreased concentrations of these amino and keto acids may be the result of decreased protein degradation or increased protein synthesis, possibly mediated by insulin.
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PMID:Effects of branched-chain amino acid antagonism in the rat on tissue amino acid and keto acid concentrations. 87 Jun 54

Temporal patterns of plasma GH, immunoreactive insulin (IRI), and glucose were defined by obtaining serial blood samples from freely-moving male rats bearing chronic intracardiac venous cannulae. Blood was withdrawn every 15 min for periods of 6 h. Plasma GH and IRI were determined by radioimmunoassay. The typical ultradian rhythm of GH secretion was evident in each undisturbed animal (peaks greater than 200 ng/ml; troughs less than 1 ng/ml; mean period: 3.40 +/-0.08 h). Basal plasma IRI and glucose levels fluctuated minimally. There was no significant correlation between plasma GH and IRI, GH and glucose, or IRI and glucose levels in unfed rats. The rhythmic GH secretory patterns of feeding animals (mean period: 3.12 +/-0.16 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) were similar to those of non-feeding animals (mean period: 3.34 +/-0.15 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) despite large fluctuations in plasma IRI levels and a wide variation in the number and size of the meals taken. No consistent relation was observed between the ingestion of meals and the bursts of GH secretion. The mean period of the GH rhythm was not significantly altered by hyperglycemia (mean period; 3.25 +/- 0.08 h), although the amplitude of the pulses of half of the hyperglycemic rats was markedly depressed. Insulin-induced hypoglycemia caused a significant depression in the amplitude of the GH pulses; however, the pattern of this response was not consistent. Despite wide variability in the GH response, the magnitude and time course of recovery of the plasma glucose levels was similar in all animals. These results suggest that GH secretion in the rat is regulated primarily by an endogenous ultradian rhythm which is not dependent on changes in plasma glucose or IRI levels, and continues to function independently of feeding behavior. It is unlikely that GH is an important physiologic regulator of glucose homeostasis in this species.
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PMID:Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia. 95 65

Lipoprotein lipase (LPL) activity was measured in adipose tissue, heart and diaphragm in Sprague--Dawley rats after estrogen therapy or orchiectomy. Enzyme activity was measured by incubation of tissue fragments with a triolein emulsion in the presence of serum and heparin. In confirmation of other work, depression of adipose tissue LPL followed estradiol treatment in pharmacologic or near-physiologic doses. Cardiac and diaphragmatic muscle LPL were increased. Estrogen-treated male animals showed growth retardation. However, they gained weight steadily and did not show significant differences in serum insulin, glucose of D-beta-hydroxybutyrate. The effects of estradiol in male animals were reversed by sequential fasting and re-feeding. At times during growth and aging in normal female rats, adipose tissue activity was decreased while cardiac and skeletal muscle activities were increased relative to males of the same age or body weight. Castration of male rats failed to reproduce the effect of estrogens on tissue lipoprotein lipase. These in vitro data suggest that exogenous estrogens may shift the flux of triglyceride fatty acids from storage in the adipose organ toward incorporation by muscle. These, and other data, raise the possibility that physiological estrogen secretion exerts a tonic influence over the synthesis and ultimate destination of triglyceride fatty acids.
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PMID:Estrogen treatment and gonadal function in the regulation of lipoprotein lipase. 97 48

The study investigated the respective influences of nicotinic acid and somatostatin on plasma concentrations of blood glucose, free fatty acids, glucagon, growth hormone and cortisol in insulin-dependent diabetic subjects. After administration of nicotinic acid alone, marked depression of plasma FFA was accompanied by significant increases of plasma glucagon, growth hormone and cortisol. The glucagon and growth hormone responses to nicotinic acid were significantly reduced when plasma FFA were raised by intravenous administration of heparin and triglycerides. Somatostatin alone induced a significant decrease in blood glucose, plasma glucagon and growth hormone concentrations. Plasma FFA remained unchanged. Somatostatin did not modify the nicotinic acid-induced fall in plasma FFA, but completely blocked the corresponding increments in glucagon and growth hormone. The cortisol rise was not altered by somatostatin. Rebound of glucagon and growth hormone levels were seen upon discontinuation of the somatostatin administration. These results demonstrate that the plasma FFA concentration plays a role in the regulation of glucagon and growth hormone secretion in insulin-dependent diabetics. Furthermore, they indicate that somatostatin, previously shown to be capable of negating the stimulatory effect of various factors on glucagon and growth hormone secretion, also affects the response of these hormones to FFA depression.
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PMID:Effect of somatostatin on metabolic and hormonal changes induced by nicotinic acid in insulin-dependent diabetics. 97 35

The effects of carbohydrate (CHO) restriction on the hypoglycemic phase of the glucose tolerance test were studied in ten normal subjects. The mean nadir plasma glucose was 64 +/- 4 mg/dl (x +/- SEM) for the control test, and 48 +/- 4 mg/dl (P less than 0.01) after 3 days of an isocaloric low CHO diet. Following the low CHO diet, six of ten subjects had a nadir plasma glucose less than 50 mg/dl, and five of these six had mild symptoms of hypoglycemia compared to no biochemical or symptomatic hypoglycemia during the control test. Hormone secretory patterns under the two experimental conditions were measured. CHO restriction produced a significant decrease in early insulin release followed by excessive insulin relative to the control test at 3-4 h of the test. Glucose ingestion produced a depression of plasma, glucagon from fasting levels during the control test, which was impaired following CHO restriction. Plasma growth hormone and cortisol responses were not different under the two experimental conditions. These studies demonstrate that CHO restriction followed by concentrated CHO ingestion produces hypoglycemia in normals. They emphasize the need to consider dietary history in evaluation of hypoglycemia. CHO restriction may provide a useful model for further study of the mechanisms of hypoglycemia.
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PMID:Effects of carbohydrate restriction on the hypoglycemic phase of the glucose tolerance test. 99 13

The effects of bilateral lesions of the ventral noradrenergic bundle (VNA) were studied in male rats. In contrast to data reported by others, hyperphagia and obesity were not observed following VNA lesions. Indeed, except for a depression during the first three postoperative days, food intake (FI) of the VNA lesioned animals (VNAL) was normal. Interestingly, the body weight (BW) of the VNAL was significantly reduced compared to the controls, and a pair feeding study indicated that this depression of BW was not due to their FI. Computation of FI per metabolic size showed that the VNAL actually had a significantly increased FI compared to the controls. After a two day fast the VNAL lost more metabolic size than controls and upon refeeding they defended their pre-fast BW. The VNAL rats showed normal body composition and circulating glucose, insulin and prolactin. They had reduced free fatty acids, triglycerides, growth hormone and body length. The data suggest that the mesencephalon influences BW set point, some metabolites and possibly overall metabolism.
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PMID:Mesencephalic lesions resulting in normophagia, reduced weight and altered metabolism. 99 50

With the aid of insulin-tolerance and arginine tolerance tests (ITT and ATT, respectively) somatotropic function of the hypophysis was assessed in 18 patients with hypophyseal nanism and in 12--with gonad dysgenesis. A marked delay in development and a premature exhaustion of the STH secretion was noted in the patients wiht hypophyseal nanism. In patients with gonad dysgenesis the STH secretion was somewhat redeced during the ITT. A change in the STH secretion was accompanied by a parallel depression of insulin secretion during the ATT. Patients with hypophyseal nanism displayed a correlation between the extent of growth delay and the value of the STH secretion during the ITT (R=0.6, P smaller than 0.05).
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PMID:[Assessment of the somatotropic function of the hypophysis in patients with hypophyseal nanism and gonadal dysgenesis by using the insulin-tolerance and arginine-tolerance tests]. 109 47

The effects of hypophysectomy and short-term GH replacement on insulin release and on some aspects of glucose metabolism in isolated rat islets of Langerhans were investigated. The effects on body, pancreas and adrenal gland weights, and on the levels of blood plasma constituents were also measured. Three to four weeks after hypophysectomy the early and late phases of insulin release from islets incubated with high concentrations of glucose, but not with low concentrations of glucose or with xylitol, leucine, arginine, tolbutamide, citrate or butyrate, were significantly lowered. Short-term GH replacement partially reversed the depression in glucose-stimulated insulin release. This reversal effect was not dependent on the increase in body weight of rats after GH replacement when the fall in adrenal gland but not in pancreas weight was also reversed. Nine out of the 12 plasma constituents measured, including glucose, were maintained in the control range of levels, but albumin, inorganic phosphate and urea nitrogen levels were altered after hypophysectomy or GH replacement. Three to four weeks after hypophysectomy, total glucose oxidation and glucose utilization by the islets were slightly depressed. Hypophysectomy appeared to slow down glucose 6-phosphate utilization in the islets. However, the functional capacity of the glucose phosphorylating, glucose-6-phosphate and 6-phosphogluconate dehydrogenase activities were not changed. Short-term GH replacement caused improvements in these islet functions.
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PMID:Effects of hypophysectomy and short-term growth hormone replacement on insulin release from and glucose metabolism in isolated rat islets of Langerhans. 110 38

A patient is described who developed hypoglycemia and generalized neurologic depression after cardiac surgery, while receiving an infusion of glucose, insulin, and potassium (GIK). Hypoglycemia as a complication of the use of GIK solution in patients with hepatic dysfunction, malnutrition and low cardiac output is discussed.
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PMID:Hypoglycemia complicating the use of solution of glucose, insulin and potassium. 111 35

This study was performed to determine whether alloxan treatment of rats alters concentrations of the terminal carbohydrate residues, L-fucose and sialic acid, of serum glycoproteins. Results indicate that in the uncompensated diabetic rat, chronic depression of serum sialic acid concentration occurred with no apparent alteration in the concentration of L-fucose. The depression in sialic acid concentration may be attributed, in part, to decreased activities of hepatic enzymes involved in sialic acid synthesis similar to those observed by others after treatment of rats with the diabetogenic agent streptozotocin. The lack of any significant alteration in the concentration of L-fucose fails to confirm, in the experimental diabetic rat, the increased protein-bound fucose values reported in human diabetics. Administration of insulin was not effective in modifying the sialic acid response after alloxan treatment.
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PMID:Chronic depression of serum concentrations of sialic acid in alloxan-induced diabetic rats. 111 28


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