1,721,003 research outputs found
On the estimation of absorption of subcutaneous injected insulin from plasma concentrations using mathematical models.
No full textThe antiketogenic effect of alanine in normal man: evidence for an alanine-ketone body cycle.
No full textThe effect of alanine on ketone body levels, independent of hormonal changes, in normal man has been investigated. Five normal subjects were given somatostatin infusions (200 micrograms/hour) for 3 hr. After 1 hr alanine or isotonic saline was infused for 2 hr. With saline blood beta-hydroxybutyrate and acetoacetate levels rose steadily to a peak of 0.230 plus or minus 0.053 and 0.112 plus or minus 0.023 mmole/l respectively. With alanine beta-hydroxybutyrate and acetoacetate levels plateaued at 0.099 plus or minus 0.020 and 0.055 plus or minus 0.006 mmole/l respectively. Alanine levels reached nearly 1 mmole/l but a significant effect on ketone body levels was apparent at physiologic levels (less than 0.6 mmole/l). Plasma fatty acid and glycerol levels did not change significantly. Insulin C-peptide and glucagon levels were suppressed to a similar extent in both experiments. These results support the view that alanine suppresses ketogenesis in man by a direct hepatic effect independent of insulin and glucagon. It is suggested that this forms part of a negative feedback substrate cycle between alanine and ketone bodies
EFFECTS OF CHRONIC ALCOHOL INTAKE ON CARBOHYDRATE AND LIPID-METABOLISM IN SUBJECTS WITH TYPE-II (NON-INSULIN-DEPENDENT) DIABETES
No full textGoing Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Hyperaminoacidaemia reduces insulin-mediated glucose disposal in healthy man.
No full textTo determine whether hyperaminoacidaemia may modify insulin-mediated glucose disposal, normal subjects were studied with the euglycaemic glucose-clamp technique, with or without an amino acid infusion, at a rate sufficient to duplicate the plasma concentration of most amino acids. Steady-state glucose infusion rates to maintain euglycaemia were 36% lower during hyperaminoacidaemia (7.3 +/- 1.0 versus 11.4 +/- 0.8 mg X kg-1 X min-1, p less than 0.01) at comparable insulin concentrations (92 +/- 6 versus 93 +/- 7 mU/l respectively). Thus, under conditions of hyperinsulinaemia, amino acids could compete with glucose as metabolic fuels
Intermediary metabolite profiles during euglycemic glucose-insulin clamp: effects of ethanol.
No full text
Glycerophosphate acetyltransferase activity in perfused liver of normal and hyperlipemic rats: glucagon effect.
No full textMitochondrial glycerophosphate-acetyltransferase activity (GPAT) was determined in the isolated and perfused liver of diet-induced hyperlipemic rats, and was found to be significantly increased compared to normal rats, A positive correlation existed between hepatic triglyceride output and GPAT. Perfusion of 10(-5) M glucagon induced a significant reduction in GPAT levels. It is suggested that the lipid-lowering action of glucagon may be mediated also through an inhibition of GPAT activity
enhanced effects of insulin and angiotensin II on intracellular pH and free cytosolic calcium in fibroblasts from microalbuminuric patients with non-insulin-dependent diabetes mellitus
No full text1. Whether an alteration in cell membrane cation transport after exposure to insulin and angiotensin II (two important growth promoters that have been shown to be involved in the pathogenesis of atherosclerosis and hypertension) is present in cells from non-insulin-dependent diabetes patients with microalbuminuria, a known risk factor for cardiovascular and renal disease, is unknown. We therefore examined intracellular pH and calcium changes after acute exposure to insulin and angiotensin II in cultured skin fibroblasts from eight non-insulin-dependent diabetes patients with and eight others without microalbuminuria and from a group of seven matched, normal control subjects. 2. Cultured fibroblasts were loaded with 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester or fura 2-acetoxymethyl ester for continuous monitoring of intracellular pH and free calcium concentrations respectively. 3. In quiescent growth-arrested cells, both intracellular pH and free calcium concentrations were similar in the three groups of subjects. Acutely, insulin induced a gradual alkalinization in all groups of patients. The pH increase was significantly greater in non-insulin-dependent diabetes mellitus patients with microalbuminuria (delta pH +0.24 +/- 0.04 pH units) than in normoalbuminuric patients with non-insulin-dependent diabetes mellitus (0.08 +/- 0.02; P < 0.01) and normal control subjects (0.05 +/- 0.01; P < 0.01). Although the alkalinizing effect of angiotensin II was smaller than that obtained by insulin, intracellular pH increase after angiotensin addition was more pronounced in non-insulin-dependent diabetes mellitus patients with microalbuminuria (delta pH +0.14 +/- 0.04 pH units) than in those without (0.08 +/- 0.02; P < 0.01) and in normal control subjects (0.02 +/- 0.02; P < 0.01). That the increase in intracellular pH was mediated by the sodium-hydrogen antiport was demonstrated by its dependence on the presence of sodium in the medium and its inhibition by amiloride. Whereas insulin addition did not evoke any significant increase in intracellular free calcium levels in fibroblasts from the three groups studied, angiotensin II evoked a fast and transient rise in intracellular free calcium that was higher in fibroblasts from microalbuminuric patients with non-insulin-dependent diabetes mellitus than in cells from normoalbuminuric patients with non-insulin-dependent diabetes mellitus and control subjects. In the whole population of patients with non-insulin-dependent diabetes mellitus, the increase in intracellular pH after exposure to angiotensin II was positively correlated with intracellular free calcium increase (r = 0.53; P < 0.05), suggesting a possible role of intracellular free calcium levels in the activation of the sodium-hydrogen antiport. 4. In conclusion, we have described an association between increased agonist-induced responsiveness of sodium-hydrogen antiport activity and the presence of microalbuminuria in patients with non-insulin-dependent diabetes mellitus. This increased responsiveness, persisting in cultured fibroblasts after several passages in vitro, suggests that in vitro phenotypic characteristics of fibroblasts are likely to be genetically determined and to be, at least in part, independent of the degree of metabolic control in vivo
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