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Query: UMLS:C0011849 (
diabetes
)
277,896
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The authors studied palmitate-1-14C metabolism in the tissues of rats with streptozotocin
diabetes
characterized by hyperglycaemia, hypoinsulinaemia and hyperlipaemia. In the tissues of diabetic animals the following changes were found in the uptake and utilization of free fatty acids: 1. In adipose tissue,
FFA
uptake and incorporation into the total adipose tissue lipids and into the
FFA
, TG, MG and DG, Pl and CHE fractions diminished. Oxidation to 14CO2 increased. 2. In the liver,
FFA
uptake and incorporation into the total liver lipids and into the
FFA
, TG, MG and DG, Pl and CHE fractions increased. Oxidation to 14CO2 remained unchanged. 3. In the diaphragm,
FFA
uptake and incorporation into the total tissue lipids and into the various lipids fractions (
FFA
, TG, MG and DG, CHE, Pl) rose. Oxidation to 14CO2 also rose. 4. The kidney displayed no changes in
FFA
metabolism from any of the metabolic aspects studied. The authors conclude that
diabetes
, in various tissues, causes changes in
FFA
metabolism which are unrelated to changes in the adipose tissue and which participate in the resultant lipid levels in the blood.
...
PMID:Metabolism of palmitate-1-14C in the tissues of rats with streptozotocin diabetes. 645 83
Nine insulin-dependent diabetics and six healthy controls were studied at rest, during, and after 60 min of bicycle exercise at a work load corresponding to 45% of their maximal oxygen intake. The catheter technique was employed to determine splanchnic and leg exchange of metabolites.
FFA
turnover and regional exchange was evaluated using [14C]oleate infusion. Basal glucose (13.8 +/- 1.1 mmol/l), ketone body (1.12 +/- 0.12 mmol/l), and
FFA
(967 +/- 110 mumol/l) concentrations were elevated in the diabetics in comparison with controls. In the resting state, splanchnic ketone acid production in the diabetics was 6-10-fold greater than in controls. Uptake of oleic acid by the splanchnic bed was increased 2-3-fold, and the proportion of splanchnic
FFA
uptake converted to ketones (61%) was threefold greater than in controls. In contrast, splanchnic fractional extraction of oleic acid was identical in diabetics and controls. A direct relationship was observed between splanchnic uptake and splanchnic inflow (plasma concentration X hepatic plasma flow) of oleic acid that could be described by the same regression line in the diabetic and control groups. During exercise, splanchnic ketone production rose in both groups. In the control group the increase in ketogenesis was associated with a rise in splanchnic inflow and in uptake of oleic acid, a rise in splanchnic fractional extraction of oleate, and an increase in the proportion of splanchnic
FFA
uptake converted to ketone acids from 20-40%. In the diabetic group, the increase in ketogenesis occurred in the absence of a rise in splanchnic inflow or uptake of oleic acid, but was associated with an increase in splanchnic fractional extraction of oleic acid and a marked increase in hepatic conversion of
FFA
to ketones, so that the entire uptake of
FFA
was accountable as ketone acid output. Splanchnic uptake of oleic acid correlated directly with splanchnic oleic acid inflow in both groups, but the slope of the regression line was steeper than in the resting state. Plasma glucagon levels were higher in the diabetic group at rest and during exercise, while plasma norepinephrine showed a twofold greater increment in response to exercise in the diabetic group (to 1,400-1,500 pg/ml). A net uptake of ketone acids by the leg was observed during exercise but could account for less than 5% of leg oxidative metabolism in the diabetics and less than 1% in controls. Despite the increase in ketogenesis during exercise, a rise in arterial ketone acid levels was not observed in the diabetics until postexercise recovery, during which sustained increments to values of 1.8-1.9 mmol/l and sustained increases in splanchnic ketone production were observed at 30-60 min. The largest increment in blood ketone acids and in splanchnic ketone production above values observed in controls thus occurred in the diabetics after 60 min of recovery from exercise. We concluded that: (a) In the resting state, increased ketogenesis in the diabetic is a consequence of augmented splanchnic inflow of
FFA
and increased intrahepatic conversion of
FFA
to ketones, but does not depend on augmented fractional extraction of circulating
FFA
by the splanchnic bed. (b) Exercise-induced increases in ketogenesis in normal subjects are due to augmented splanchnic inflow and fractional extraction of
FFA
as well as increased intrahepatic conversion of
FFA
to ketones. (c) When exercise and
diabetes
are combined, ketogenesis increases further despite the absence of a rise in splanchnic inflow of
FFA
. An increase in splanchnic fractional extraction of
FFA
and a marked increase intrahepatic conversion of
FFA
to ketones accounts for the exaggerated ketogenic response to exercise in the diabetic. (d) Elevated levels of plasma glucagon and/or norepinephrine may account for the increased hepatic ketogenic response to exercise in the diabetic. (e) Ketone utilization by muscle increases during exercise but constitutes a quantitatively minor oxidative fuel for muscle even in the diabetic. (f) The accelerated ketogenesis during exercise in the diabetic continues unabated during the recovery period, resulting in an exaggerated postexercise ketosis.
...
PMID:Turnover and splanchnic metabolism of free fatty acids and ketones in insulin-dependent diabetics at rest and in response to exercise. 671 41
The aim of the present study is to determine the "in vitro" rate of 1-14C-acetate incorporation into lipids in human liver slices from patients with various types of hyperlipoproteinemia. Hepatic tissue from type IIa hyperlipemic patients incorporated labelled acetate into free cholesterol at a higher rate than normolipidemic patients. In type IIb patients the incorporation was increased into hepatic free cholesterol, triglycerides and
FFA
. The liver of pre-beta hyperlipoproteinemic subjects incorporated 1-14C-acetate into triglycerides to a greater extent than hepatic tissue from controls. Triglyceride synthesis was highly elevated in type IV hyperlipoproteinemic patients with
diabetes
. In all cases, there was no significant correlation between increased hepatic triglyceride synthesis (dpm/mg of extracted lipids) and insulin response (microunits/ml) to oral glucose ingestion (75 g). The present data indicates that in the presence of disturbances in lipid and carbohydrate metabolism one observes an alteration of lipid synthesis in the liver. The in vitro incorporation of 1-14C-acetate into hepatic cholesterol and/or triglyceride in patients with primary hyperlipoproteinemia is increased. Thus the elevated serum cholesterol and triglyceride levels of these patients could be explained on the basis of an increased lipoprotein synthesis in the liver.
...
PMID:In vitro study of liver slices lipid 1-14C-acetate incorporation in hyperlipoproteinemic subjects. 675 76
The relationship between insulin concentrations and insulin effects was assessed using a 30-min steady-state perfusion of insulin across the human forearm and a 90-min recovery period in 17 normal men. During perfusion, calculated insulin increments in forearm arterial plasma insulin were 87 +/- 4 (group I), 161 +/- 17 (group II), and 333 +/- 55 microU/ml (group III), respectively. Measured venous insulin increments were 33 +/- 4, 66 +/- 6, and 231 +/- 27 microU/ml. During perfusion, venous and arterial increments were linearly related (r = 0.88, P less than 0.001). With discontinuation of perfusion, venous increments of insulin became undetectable after 15 min in groups I and II, and after 30 min in group III. Of the total microunits of insulin perfused, 46.0 +/- 11.0%, 45.3 +/- 9.4%, and 36.5 +/- 4.8%, respectively, remained unaccounted for 90 min after perfusion. Effects of insulin on arteriovenous differences of
FFA
and potassium persisted throughout the recovery period, with peak effects occurring after perfusion for all groups. Estimated interstitial insulin levels in the three groups fell below 10 microU/ml by 45, 60, and 90 min after perfusion, respectively. Although peripheral tissues had a significant capacity to sequester insulin, the persistence of biologic effects was not consistent with increased concentrations within the interstitial spaces. Effects of insulin upon glucose waned first, followed by effects upon potassium and then lipolysis.
Diabetes
Care
PMID:Studies on the relationship between insulin concentrations and insulin action. 675 38
Thyroid hormone abnormalities in serum were investigated in 47 patients with
diabetes mellitus
. Although no significant differences in T4 were found between normal subjects and diabetics, a group of diabetics whose fasting blood sugar levels were over 250 mg/dl showed significantly higher reverse T3 (rT3) (p less than 0.01) and lower T3 levels (p less than 0.05) than healthy controls. A significant correlation was observed between rT3 and
FFA
levels in diabetics. Moreover, patients in diabetic ketoacidosis showed markedly high rT3 with low T3 levels. With insulin treatment, these levels returned to normal in several days. These findings suggest that the reduction of T3 and the increase of rT3 may indicate an adaptation to limit catabolism in diabetics.
...
PMID:Thyroid hormone abnormalities in patients with diabetes mellitus. 678 11
In New Zealand rabbits a single intravenous injection of streptozotocin (STZ 65 mg/kg) elevated the levels of blood sugar to 340 mg percent, which was associated with glycolysis, ureamia, hypercholesterolemia, hypertriglyceridemia and loss of body weight. Oral administration of jambolan seed (1 g/kg) in casein diet significantly lowered the elevated postmeal (1 1/2 hr after) values of blood sugar, cholesterol,
FFA
and triglyceride down to levels comparable to phenformin. Jambolan seed treatment failed to check ureamia. Weight loss was checked by phenformin and jambolan seed but the gain was not equivalent to that recorded in nondiabetic control. Like phenformin, jambolan seed too failed to control glycogenolysis in STZ-induced
diabetes
.
...
PMID:Effects of jambolan seed treatment on blood sugar, lipids and urea in streptozotocin induced diabetes in rabbits. 688 26
Twenty-three normal weight subjects without any heredity of
diabetes
were characterized by a 2-hour glucose infusion test. All persons showed a normal carbohydrate tolerance and normal biphasic insulin secretion pattern. For the determination of insulin sensitivity a 1-hour priming dose--constant infusion technique was used. Two 30-minute-periods of insulin infusion (8 and 16 mU/kg, primed by a start injection of 1 and 2 mU/kg, respectively) provoked a decrease of plasma glucose and
FFA
concentrations by 35 +/- 12.5% and 55 +/- 30.2%, respectively. Values lower than 22.5% (glycemia) or 25% (
FFA
) indicate a diminished insulin responsiveness. The metabolic clearance rate of insulin did not change at several concentrations of IRI. Thus, the proposed procedure is suitable to study the insulin sensitivity in vivo.
...
PMID:Investigation of insulin sensitivity in early diabetes. I. Procedure for the determination of insulin responsiveness in vivo. 698 94
This study aimed at evaluating the effect of acetylsalicylic acid (ASA) on blood glucose, plasma
FFA
, glycerol, 3-hydroxybutyrate, alanine, C-peptide, glucagon and growth hormone responses to arginine in subjects with insulin-dependent
diabetes
. For this purpose, seven insulin-requiring diabetics were submitted to a standard arginine tolerance test before and after a three day treatment with ASA (50 mg/kg/daily, plus 1 g before the second test). ASA treatment resulted in no significant changes in either basal or arginine-stimulated blood glucose, but it significantly decreased the basal concentrations of plasma
FFA
(p less than 0.05), 3-hydroxybutyrate (p less than 0.05) and glycerol (p less than 0.05). In addition, the fall in plasma
FFA
concentrations during arginine infusion was significantly less after ASA than levels observed without ASA (--262 +/- 100 microEq/l vs --35 +/- 57 microEq/l, p less than 0.02). No significant changes in either basal or arginine-stimulated glucagon concentrations were observed after ASA; by contrast, the growth hormone peak was significantly reduced after ASA (11.3 +/- 4.2 ng/ml vs 5.1 +/- 1.1 ng/ml, p less than 0.05). These metabolic effects exerted by ASA in insulin-dependent
diabetes
seem not to be related to alterations in endogenously secreted insulin since C-peptide circulating levels were similar during the pre- and post-treatment arginine tests.
...
PMID:Effects of acetylsalicylic acid on blood glucose, plasma FFA, glycerol, 3-hydroxybutyrate, alanine, C-peptide, glucagon and growth hormone responses to arginine in insulin-dependent diabetics. 698 60
In normal dogs epinephrine stimulates glucose production (Ra) independently of glucagon. To investigate the role of this interaction in
diabetes
, epinephrine (0.1 micrograms . kg-1 . min-1) was infused for 90 min in five alloxan-diabetic dogs in the presence or absence of somatostatin (0.1 micrograms . kg-1 . min-1). In response to epinephrine, glycemia rose by 40% reflecting a near maximal (122%) increase in Ra. Plasma glucagon (IRG) rose to 953 pg/ml, whereas insulin (IRI) increased minimally. When somatostatin was infused with epinephrine to prevent the rise of IRG and IRI, there was only a marginal increase of glucose concentration (12%) and production (38%). The effect of somatostatin was reversed by infusing glucagon (10 ng . kg-1 . min-1) together with epinephrine and somatostatin into five additional alloxan-diabetic dogs. Increments in IRG, glycemia, and Ra were fully reestablished. A 100%
FFA
increase was observed in all three groups, indicating that the lipolytic effect of epinephrine was independent of glucagon. In conclusion, in diabetic dogs, in contrast to normal dogs, epinephrine induced a marked and prolonged increase in glucose concentration and production mostly through a stimulation of IRG secretion.
...
PMID:Importance of glucagon in mediating epinephrine-induced hyperglycemia in alloxan-diabetic dogs. 703 19
Adipose tissue lipoprotein lipase (ATLPL) is responsible for the provision of lipoprotein-derived fatty acids to adipocytes for storage as triglycerides. Fasting ATLPL has been shown to be decreased in non-insulin-dependent
diabetes mellitus
(NIDDM), an insulin-resistant state. Medically uncomplicated obesity, another state of relative insulin resistance, is associated with decreased stimulation of the enzyme in response to metabolic stimuli. It was therefore hypothesized that the increased insulin resistance of NIDDM would result in an even greater defect in the response of ATLPL to insulin/glucose. Gluteal adipose tissue biopsies were performed in 13 premenopausal obese women with NIDDM, before and after 6 hours of intravenous insulin and glucose. Metabolic data from these studies were then compared with those obtained from 26 nondiabetic obese women of similar age, weight, and fasting insulin concentration (obese controls [OBC]). As expected, fasting gluteal ATLPL activity was lower in the NIDDM group than in OBC (3.7 +/- 0.9 v 11.1 +/- 1.6 nmol free fatty acids [
FFA
]/min/10(6) cells, P = .0003). The change in ATLPL activity (delta ATLPL) in response to a 6-hour insulin/glucose infusion was not statistically different between the two groups (2.2 +/- 1.1 v 4.7 +/- 1.2, P = .114). However, in NIDDM subjects there was a strong positive relationship between delta ATLPL and glycohemoglobin (GHb) level (r = .883, P = .0001).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Glycohemoglobin levels relate to the response of adipose tissue lipoprotein lipase to insulin/glucose in obese non-insulin-dependent diabetes mellitus. 747 37
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