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  • 1
    Electronic Resource
    Electronic Resource
    Are the binding and degradation of low density lipoprotein altered in type 2 (non-insulin-dependent) diabetes mellitus? (1982)
    Springer
    Diabetologia 23 (1982), S. 28-33 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 diabetes mellitus ; low density lipoprotein ; lipoprotein binding ; lipoprotein degradation ; fibroblast, macrophage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Studies in vitro have shown that glycosylation of low density lipoprotein (LDL) will decrease its ability to bind to its receptor. We have evaluated the possibility that such an event might occur in vivo in diabetes by comparing the binding and degradation by normal fibroblasts and mouse peritoneal macrophages of LDL obtained from normal control subjects and patients with Type 2 (non-insulin-dependent) diabetes mellitus. When compared with control subjects, Type 2 diabetic patients had elevated fasting glucose (increased by 160%), haemoglobin A1c (increased by 75%), triglyceride (increased by 550%), and cholesterol (increased by 48%) levels. LDL from Type 2 diabetic patients displayed populations of particles with more heterogeneous hydrated densities than LDL from control subjects, with enrichment in the triglyceride content of the lighter population. 125I-LDL from normal and Type 2 diabetic subjects bound to fibroblasts with similar binding affinities and binding capacities. The kinetics of degradation of LDL from normal and Type 2 diabetic subjects by fibroblasts were also similar. Furthermore, all populations of LDL particles from Type 2 diabetic patients were bound and degraded by normal fibroblasts in identical fashions. In addition, 125I-LDL from normal and Type 2 diabetic subjects were not bound or degraded by mouse peritoneal macrophages. It is concluded that the LDL of patients with Type 2 diabetes with moderate hyperglycaemia are not modified sufficiently to alter their normal binding and degradation by human fibroblasts or to cause their uptake by mouse peritoneal macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00257726
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  • 2
    Electronic Resource
    Electronic Resource
    Relationship between glucose tolerance, insulin secretion, and insulin action in non-obese individuals with varying degrees of glucose tolerance (1989)
    Springer
    Diabetologia 32 (1989), S. 52-55 
    Details
    ISSN: 1432-0428
    Keywords: Type 2 diabetes ; impaired glucose tolerance ; insulin resistance ; insulin response ; glucose tolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma glucose and insulin concentration following a 75 g oral glucose challenge and glucose uptake during a hyperinsulinaemic glucose clamp study were determined in 50 non-obese individuals. The study population was divided into five groups on the basis of their glucose tolerance: normal, impaired glucose tolerance, Type 2 (non-insulin-dependent) diabetes mellitus with fasting plasma glucose of less than 8 mmol/l, between 8–15 mmol/l, and more than 15 mmol/l. The plasma insulin response was significantly greater (p〈0.001) than normal in those with either impaired glucose tolerance or Type 2 diabetes and a fasting plasma glucose concentration less than 8 mmol/l. In contrast, the plasma insulin response was similar to normal in the other two groups of patients with Type 2 diabetes, i.e. fasting plasma glucose concentration 8–15 mmol/l or greater than 15 mmol/l. Glucose uptake rates were significantly lower (p〈0.001) than normal in subjects with impaired glucose tolerance and all three groups of patients with Type 2 diabetes. Although glucose uptake rates during the glucose clamp studies were relatively similar in all four groups of glucose intolerant subjects, the values were significantly lower in those patients with Type 2 diabetes who had a fasting plasma glucose concentration greater than 8 mmol/l (p〈0.01), These data indicate that a significant degree of insulin resistance exists in patients with impaired glucose tolerance or Type 2 diabetes, relatively independent of fasting plasma glucose concentration. Indeed, glucose uptake during glucose clamp studies fell 8-fold over a range in fasting plasma glucose concentration of from 4.5 to 6.5 mmol/l. In contrast, the plasma insulin response increased over the same range of fasting plasma glucose concentrations. The fact that this defect in insulin action can be seen in patients who are hyperinsulinaemic, not hypoinsulinaemic, and only modestly hyperglycaemic, is consistent with the hypothesis that resistance to insulin-stimulate glucose uptake is a basic characteristic of patients with impaired glucose tolerance or Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265404
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  • 3
    Electronic Resource
    Electronic Resource
    Evidence that insulin can directly inhibit hepatic glucose production (1997)
    Springer
    Diabetologia 40 (1997), S. 1300-1306 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Liver ; insulin ; portal system ; C-peptide ; tolbutamide.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to evaluate the role of portal insulin in the modulation of hepatic glucose production (HGP), measurements of plasma glucose and insulin concentrations and both HGP and peripheral glucose disappearance rates were made following an infusion of a dose of tolbutamide (0.74 mg · m−2· min−1) in healthy volunteers that does not result in an increase in peripheral vein insulin concentrations or metabolic clearance rate of glucose. The results showed that the infusion of such a dose of tolbutamide was associated with a significant and rapid decline in both HGP (from 9.0 ± 0.5 to 7.7 ± 0.5 μmol · kg−1· min−1 or Δ = − 13.8 ± 4.5 %; p 〈 0.001 compared to saline) and plasma glucose concentration (from 5.1 ± 0.2 to 4.4 ± 0.1 mmol/l or Δ = − 13.0 ± 2.1 %; p 〈 0.01 compared to saline). Since neither HGP nor fasting glucose fell when tolbutamide-stimulated insulin secretion was inhibited by the concurrent administration of somatostatin, it indicated that tolbutamide by itself, does not directly inhibit HGP. Finally, HGP fell by 26.3 ± 6.0 % at 10 min after a dose of tolbutamide that elevated both peripheral and portal insulin concentrations, at a time when HGP had barely increased (Δ = + 6.9 ± 5.3 %). The difference in the magnitude of the two responses was statistically significant (p 〈 0.03), providing further support for the view that insulin can directly inhibit HGP, independent of any change in flow of substrates from periphery to liver. [Diabetologia (1997) 40: 1300–1306]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050824
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 781-787 
    Details
    ISSN: 1432-0428
    Keywords: Key words Intestinal lipoproteins, Sf 〉400 fraction, Sf 20–400 fraction, insulin resistance, insulin suppression test, steady-state plasma glucose, steady-state plasma insulin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The primary goal of the present study was to examine the effects of improved glycaemic control associated with glipizide treatment on postprandial lipaemia in non-insulin-dependent diabetic patients. The metabolism of triglyceride-rich lipoproteins of intestinal origin was assessed by measuring the retinyl palmitate content in plasma and the Svedberg flotation index (Sf) 〉400 and Sf 20–400 lipoprotein fractions. Fasting plasma glucose concentrations (14.5±0.5 vs 9.0±0.5 mmol/l), glycated haemoglobin levels (13.1± 0.6 vs 9.7±0.6 %), and daylong plasma glucose concentrations were all significantly lower after glipizide treatment (p〈0.001). The improvement in glycaemic control was associated with increases in insulin-mediated glucose uptake (p〈0.001) and plasma post-heparin lipoprotein and hepatic lipolytic activities (p〈0.02). Both fasting plasma triglyceride (3.09±0.51 vs 2.37± 0.34 mmol/l), and postprandial triglyceride concentrations (p〈0.05–0.001) were lower following glipizide treatment, associated with a significant fall in retinyl palmitate content in all three lipoprotein fractions (p〈0.02–0.001), with the most substantial decrease seen in the Sf 20–400 fraction. These data indicate that glipizide-induced improvement in glycaemic control was associated with changes in the metabolism of triglyceride-rich lipoproteins of intestinal origin that would be anticipated to reduce risk of coronary heart disease in non-insulin-dependent diabetic patients. [Diabetologia (1994) 37: 783–787]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404335
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of glipizide treatment on postprandial lipaemia in patients with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 781-787 
    Details
    ISSN: 1432-0428
    Keywords: Intestinal lipoproteins ; Sf〉400 fraction ; Sf 20–400 fraction ; insulin resistance ; insulin suppression test ; steady-state plasma glucose ; steady-state plasma insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The primary goal of the present study was to examine the effects of improved glycaemic control associated with glipizide treatment on postprandial lipaemia in non-insulin-dependent diabetic patients. The metabolism of triglyceride-rich lipoproteins of intestinal origin was assessed by measuring the retinyl palmitate content in plasma and the Svedberg flotation index (Sf)〉400 and Sf 20–400 lipoprotein fractions. Fasting plasma glucose concentrations (14.5±0.5 vs 9.0±0.5 mmol/l), glycated haemoglobin levels (13.1±0.6 vs 9.7±0.6%), and daylong plasma glucose concentrations were all significantly lower after glipizide treatment (p〈0.001). The improvement in glycaemic control was associated with increases in insulin-mediated glucose uptake (p〈0.001) and plasma post-heparin lipoprotein and hepatic lipolytic activities (p〈0.02). Both fasting plasma triglyceride (3.09±0.51 vs 2.37±0.34 mmol/l), and postprandial triglyceride concentrations (p〈0.05–0.001) were lower following glipizide treatment, associated with a significant fall in retinyl palmitate content in all three lipoprotein fractions (p〈0.02–0.001), with the most substantial decrease seen in the Sf 20–400 fraction. These data indicate that glipizide-induced improvement in glycaemic control was associated with changes in the metabolism of triglyceride-rich lipoproteins of intestinal origin that would be anticipated to reduce risk of coronary heart disease in non-insulin-dependent diabetic patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404335
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Relationship between insulin-mediated glucose disposal and regulation of plasma and adipose tissue lipoprotein lipase (1997)
    Springer
    Diabetologia 40 (1997), S. 850-858 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Lipoprotein lipase ; insulin resistance ; adipose tissue ; RNA messenger ; triglycerides.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between insulin-mediated glucose disposal and fasting insulin and triglyceride (TG) concentrations, plasma post-heparin lipoprotein lipase (PH-LPL) activity and mass, and adipose tissue LPL activity, mass, and mRNA content was defined in 19 non-diabetic men. Insulin-mediated glucose uptake [as assessed by determining the steady-state plasma glucose (SSPG) concentration during a continuous infusion of somatostatin, insulin, and glucose] was significantly correlated with fasting TG concentration (r = 0.54, p 〈 0.02), plasma PH-LPL activity (r = –0.52, p 〈 0.03) and mass (r = –0.49, p 〈 0.03), and adipose tissue LPL mRNA content (r = –0.68, p 〈 0.001). Comparable relationships were also seen when fasting insulin concentration was substituted for SSPG. Although adipose tissue LPL and mass correlated with each other (r = 0.76, p 〈 0.001) in a fasting state, they were not related to any other variable measured. Using in vivo and molecular biology techniques, these data demonstrate that the more insulin resistant an individual, the lower the level of plasma PH-LPL activity and mass, and the higher the plasma TG concentration. Since lower concentrations of adipose tissue mRNA were also directly correlated with plasma PH-LPL mass (r = 0.57, p 〈 0.01), and inversely with plasma TG concentration (r = –0.68, p 〈 0.001) as well as SSPG (r = –0.68, p 〈 0.001), it can be postulated that the relationship between insulin resistance and LPL activity and plasma TG concentration is associated with the inability of insulin to stimulate the transcription or to increase the intracellular mRNA stability of adipose tissue LPL in insulin resistant individuals. [Diabetologia (1997) 40: 850–858]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050759
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  • 7
    Electronic Resource
    Electronic Resource
    Evaluation of octreotide to assess insulin-mediated glucose disposal by the insulin suppression test (1994)
    Springer
    Diabetologia 37 (1994), S. 843-845 
    Details
    ISSN: 1432-0428
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404344
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  • 8
    Electronic Resource
    Electronic Resource
    Insulin suppression of plasma-free fatty acid concentration in normal individuals and patients with Type 2 (non-insulin-dependent) diabetes (1987)
    Springer
    Diabetologia 30 (1987), S. 622-626 
    Details
    ISSN: 1432-0428
    Keywords: Free fatty acid ; Type 2 (non-insulin-dependent) diabetes ; insulin suppression ; insulin dose-response curve
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to define the effect of Type 2 (non-insulin-dependent) diabetes mellitus on the ability of insulin to regulate plasma-free fatty acid (FFA) concentrations, we determined the plasma FFA response to the intravenous infusion of various amounts of insulin. Plasma FFA concentrations were higher in patients with Type 2 diabetes (two way analysis of variance, p〈0.001) over a plasma insulin concentration which ranged from approximately 5 to 55 mU/l of insulin. Although plasma FFA concentrations were higher in patients with Type 2 diabetes at any given insulin concentration, the relative ability of insulin to suppress plasma FFA concentration to half the initial value was comparable in normal individuals and patients with Type 2 diabetes, occurring at a plasma insulin concentration of approximately 20 mU/l. These data demonstrate that plasma FFA levels are regulated over a narrow range of plasma insulin concentrations in humans, and that plasma concentrations are higher than normal in patients with Type 2 diabetes throughout this range.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277318
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