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  • 1
    Electronic Resource
    Electronic Resource
    Increased ketonaemia in hyperthyroidism (1980)
    Springer
    Diabetologia 19 (1980), S. 505-510 
    Details
    ISSN: 1432-0428
    Keywords: Hyperthyroidism ; blood ketone bodies ; glycerol ; catecholamines ; starvation ; β-blockade
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The metabolic status of 16 hyperthyroid patients and 22 control subjects was studied in the post-absorptive state after 3 days on a standard diet (35 kcal/kg body weight/day). In hyperthyroidism the ranges of blood ketone body (19–1159 vs 17–233 μmol/l, p〈0.001) and glycerol (59–285 vs 15–69 μmol/l, p〈0.001) concentrations were increased relative to controls despite slight hyperglycaemia (4.9±0.6 vs 4.6±0.4 mmol/l, mean±SD p〈0.05). Plasma non-esterified fatty acids, immunoreactive insulin and glucagon levels were not significantly different. A positive correlation was found between thyroid hormone and ketone body (p〈0.02) and glycerol (p〈0.05) levels and between glycerol and ketone bodies (p〈0.05). There was no correlation of non-esterified fatty acids with either thyroid hormone or ketone body concentrations. In hyperthyroid patients propranolol administration for 4 days induced a decrease in triiodothyronine (349±140 to 229±107 ng/100ml, p〈0.01) and a dramatic fall in ketone body (18–295 μmol/l, p〈0.001) and glycerol (44–130 μmol/l, p〈0.001) levels. Non esterified fatty acids were unchanged. There was no longer a correlation between thyroid hormones and ketone bodies or glycerol. Placebo administration to 6 other hyperthyroid patients had no significant effect. In euthyroid obese subjects on a 600 kcal/day diet, propranolol administration did not change ketone body or glycerol levels. These data provide evidence for an increase in both lipolysis and ketogenesis in hyperthyroidism which might, at least in part, be dependent upon a catecholamine β-receptor mediated mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253176
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  • 2
    Electronic Resource
    Electronic Resource
    The contribution of naturally labelled 13C fructose to glucose appearance in humans (1993)
    Springer
    Diabetologia 36 (1993), S. 338-345 
    Details
    ISSN: 1432-0428
    Keywords: Fructose ; glucose ; stable isotopes ; [13C] ; mass spectrometry ; nutrition ; human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Among monosaccharides, fructose has a small hyperglycaemic effect. In order to better explain the mechanisms which cause this metabolic property, we used tracers labelled with stable isotopes (deuterated glucose and naturally 13C labelled fructose) to quantify the overall glucose appearance, the rate of appearance in plasma of the 13C glucose synthesized from fructose, and the fructose oxidation in vivo in man during a 6-h period following ingestion of 0.5 and 1 g · kg−1 fructose. Fructose had a very small effect on overall glucose appearance (NS). During the 6 h of the study, it was found that the overall glucose appearance was 0.87±0.06 and 0.89±0.06 g · kg−1 (NS). The amount of glucose synthesized from fructose was 0.27±0.04 and 0.51±0.03 g · kg−1 (p〈0.01) representing 31% and 57% of overall glucose appearance (p〈0.01); the non-fructose glucose production was 0.60±0.02 and 0.38±0.03 g · kg−1 (p〈0.05) after the 0.5 and 1 g · kg−1 load, respectively. Fructose oxidation was 0.28±0.03 and 0.59±0.07 g · kg−1 after the 0.5 and 1 g · kg−1 load respectively (p〈0.01) representing 56% and 59% of the fructose loads (NS). These data show that the low hyperglycaemic effect of fructose is explained by its very small effect on overall glucose appearance and that fructose has a sparing effect on glucose metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400238
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  • 3
    Electronic Resource
    Electronic Resource
    Defective regulation of phosphatidylinositol-3-kinase gene expression in skeletal muscle and adipose tissue of non-insulin-dependent diabetes mellitus patients (1999)
    Springer
    Diabetologia 42 (1999), S. 358-364 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Hyperinsulinaemic clamp ; insulin receptor ; IRS-1 ; RT-PCR.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the regulation of the mRNA expression of the insulin receptor, insulin receptor substrate-1 (IRS-1) and p85α-phosphatidylinositol-3-kinase (PI-3K), three major actors of insulin action, in skeletal muscle from 10 healthy lean volunteers, 13 obese patients with Type II (non-insulin-dependent) diabetes mellitus and 7 non-diabetic obese subjects. The in vivo regulation by insulin was studied using a 3-h euglycaemic, hyperinsulinaemic clamp. There were no differences in the basal concentrations of the three mRNAs in skeletal muscle between groups. Insulin infusion produced a twofold reduction in insulin receptor substrate-1 mRNA expression in the three groups (p 〈 0.02). In contrast, insulin increased p85α-phosphatidylinositol-3-kinase mRNA expression in muscle from non-diabetic subjects ( + 98 ± 22 % in lean and + 127 ± 16 % in obese, p 〈 0.02) but this effect was totally impaired in Type II diabetic patients ( + 5 ± 12 %, NS). A similar defect in insulin action on p85α-phosphatidylinositol-3-kinase mRNA expression was observed in abdominal subcutaneous adipose tissue ( + 138 ± 25 %, p 〈 0.01 in lean and + 46 ± 14 %, p 〈 0.02 in obese and + 29 ± 11 %, NS in Type II diabetic patients). The lack of action of insulin on p85α-phosphatidylinositol-3-kinase mRNA in diabetic subjects was probably not due to a deleterious effect of hyperglycaemia since improvement of the glycaemic control for 10 days did not restore the response in muscle or in adipose tissue. This study provides evidence for a defect in the regulation by insulin of PI-3K gene expression in Type II diabetic patients, thus reinforcing the concept that alterations at the gene expression might be involved in the pathogeny of Type II diabetes. [Diabetologia (1999) 42: 358–364]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051163
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  • 4
    Electronic Resource
    Electronic Resource
    Endogenous glucose production, gluconeogenesis and liver glycogen concentration in obese non-diabetic patients (1997)
    Springer
    Diabetologia 40 (1997), S. 463-468 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Substrate oxidation ; glycogenolysis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Resting, post-absorptive endogenous glucose production (EGP), fractional gluconeogenesis and liver glycogen concentration were assessed in 6 lean and 5 obese non-diabetic subjects undergoing elective abdominal surgery. During the 2 days preceding these measurements, 0.3 g/day U-13C glucose had been added to their usual diet to label their endogenous glycogen stores. On the morning of day 3, EGP was measured with 6,6-2H glucose. Their endogenous 13C glycogen enrichment was calculated from 13CO2 and respiratory gas exchanges. Fractional gluconeogenesis was assessed as 1-(13C glucose/13C glycogen) · 100. EGP was similar in lean subjects (113 ± 5 mg/min) and in obese subjects (111 ± 6). Fractional gluconeogenesis was higher in obese (59 ± 10 %) than in lean subjects (29 ± 8 %). However, overall EGP remained constant due to a decrease in glycogenolysis. Since an increased gluconeogenesis and a decreased glycogenolysis may both contribute to increase liver glycogen concentration in obesity, hepatic glycogen concentrations were assessed in hepatic needle biopsies obtained during surgery. Hepatic glycogen concentrations were increased in obese patients (515 ± 38 mg/g protein) compared to lean subjects (308 ± 58, p 〈 0.05). It is concluded that in obese patients: a) fractional gluconeogenesis is increased; b) overall EGP is unchanged due to a proportional inhibition of glycogenolysis; c) liver glycogen concentration is increased. [Diabetologia (1997) 40: 463–468]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050701
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of gene expression during severe caloric restriction: lack of induction of p85alpha phosphatidylinositol 3-kinase mRNA in skeletal muscle of patients with Type II (non-insulin-dependent) diabetes mellitus (2000)
    Springer
    Diabetologia 43 (2000), S. 356-363 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Phosphatidylinositol-3-kinase, insulin receptor, Rad, hexokinase II, GLUT 4, lipoprotein lipase, insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Alterations in the regulation of gene expression could be involved in the development of Type II (non-insulin-dependent) diabetes mellitus.¶Methods. We compared the mRNA concentrations of eight genes encoding proteins involved in insulin action and intermediary metabolism in skeletal muscle of healthy volunteers and Type II diabetic patients. The in vivo regulation of the expression of these genes was investigated after 5 days of hypocaloric diet (1045 kJ/day).¶Results. In the basal state, diabetic muscle showed reduced insulin receptor (–38 %), hexokinase II (–73 %), glycogen synthase (–45 %) and lipoprotein lipase (–70 %) mRNA expression. There was no difference in the mRNA abundances of IRS-1, GLUT 4, p85α phosphatidylinositol-3-kinase (p85αPI3K) or Rad. In both groups, caloric restriction induced weight loss, reduced glycaemia and increased plasma ketone body concentrations. The diet also increased plasma concentrations of fatty acids and decreased whole-body insulin sensitivity in control subjects. In control subjects, the diet increased p85αPI3K ( + 146 %), insulin receptor ( + 100 %) and Rad ( + 40 %) mRNA concentrations in muscle. In Type II diabetic patients, the diet increased insulin receptor ( + 41 %) and Rad ( + 31 %) mRNAs but the expression of p85αPI3K was not modified.¶Conclusion/interpretation. The regulation of the expression of p85αPI3K is altered during caloric restriction in skeletal muscle of Type II diabetic patients. Because we have shown in an earlier study that there is also a defective regulation of p85αPI3K gene expression in response to insulin, these data support the hypothesis that alterations in the regulation of gene expression could be involved in the pathogenesis of Type II diabetes. [Diabetologia (2000) 43: 356–363]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050054
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  • 6
    Electronic Resource
    Electronic Resource
    Use of compounds naturally labeled with stable isotopes for the study of the metabolism of glycoprotein neutral sugars by gas-liquid chromatography-isotope-ratio mass spectrometry. Technical validation in the rat
    Amsterdam : Elsevier
    Carbohydrate Research 236 (1992), S. 29-37 
    Details
    ISSN: 0008-6215
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0008-6215(92)85005-K
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  • 7
    Electronic Resource
    Electronic Resource
    Cyclic AMP-dependent phosphorylation of high molecular mass proteins in pig thyroid cells
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 44 (1986), S. 251-260 
    Details
    ISSN: 0303-7207
    Keywords: cAMP-dependent protein kinase ; phosphorylation ; thyroid cell
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0303-7207(86)90131-0
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  • 8
    Electronic Resource
    Electronic Resource
    Determination of human ketone body kinetics using stable-isotope labelled tracers (1986)
    Springer
    Diabetologia 29 (1986), S. 90-96 
    Details
    ISSN: 1432-0428
    Keywords: Acetoacetate ; β-hydroxybutyrate ; ketogenesis ; ketone body kinetics ; stable isotopes ; mass spectrometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to avoid the use of radioactive tracers for the determination of human ketone body turnover, we have developed a method using a primed-continuous infusion of 13C-labelled acetoacetate or D-β-hydroxybutyrate. Determination of the mole percent enrichment of blood acetoacetate and D-β-hydroxybutyrate was performed by gas chromatography/mass spectrometry. In the post-absorptive state, the mean total ketone body appearance rate, determined in four subjects, was 3.74 μmol · kg−1 · min−1 using [3,4-13 C2] acetoacetate and 2.76 μmol · kg−1 · min−1 using [3-13C]D-β-hydroxybutyrate, values in agreement with those reported in studies with 14C-labelled tracers. In order to evaluate the usefulness of the method for determination of ketone body kinetics in non steady-state conditions, we infused four subjects with natural sodium acetoacetate and calculated the isotopically determined total ketone body appearance rate using a single compartment model (volume of distribution 0.201/kg; functional pool fraction: 1). During the tests with [3,4-13C2]-acetoacetate, the actual infusion rates of natural acetoacetate were 7.3±0.3, 14.6±0.8, 21.9±1.2 and 10.9 ± 0.6 μ mol · kg−1 · min−1 whereas the corresponding isotopically determined total ketone body appearance rates were respectively 9.2±1.0, 16.3±0.7, 23.1±1.1 and 10.7±0.8 μmol· kg−1 · min−1. During the tests with [3-13C]D-β-hydroxybutyrate, the actual infusion rates were 8.4 ± 0.5, 16.8 ± 0.9, 25.2 ±1.4 and 12.6±0.8 μmol · kg−1 · min−1, and the isotopically determined appearance rates respectively 11.1±0.7, 16.7±0.7, 25.0±1.1 and 11.1 ± 0.7 μmol · kg−1 · min−1. Thus, using either tracer we found a good agreement between acetoacetate infusion rate and tracer-determined appearance rate of ketone bodies. In conclusion, the present method may be used to determine human ketone body kinetics under steady-state and non steady-state conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00456116
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  • 9
    Electronic Resource
    Electronic Resource
    Use of a new gas chromatograph isotope ratio mass spectrometer to trace exogenous 13C labelled glucose at a very low level of enrichment in man (1990)
    Springer
    Diabetologia 33 (1990), S. 449-456 
    Details
    ISSN: 1432-0428
    Keywords: Stable isotope ; [13C] glucose ; mass spectrometry ; human ; oral glucose load ; gas chromatography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The use of 13C labelled glucose in human metabolic studies has been limited by the high cost of the tracer and the problems of measuring low 13C isotopic abundance in plasma glucose. In the present work we describe a new gas chromatograph-isotope ratio mass spectrometer allowing the measurement of a 0.001 atom % increase in 13C abundance over baseline, on a nanomole glucose sample. Studies were performed in rats and in human subjects. The rate of glucose appearance in 24 h fasted rats using D-[1-13C] glucose as tracer and analysed by this new method was found to be 10.4±0.7 mg·kg−1· min−1, a value 21% lower than that found using D-[6,6-2H2] glucose as tracer (13.1±1.1 mg· kg−1· min−1) analysed by classic gas chromatography-mass spectrometry. The new method was also used to trace, in combination with D-[6,6 2H2] glucose, the metabolic fate in human subjects of two oral glucose loads (0.5 g· kg·−1), 1 g· kg ·−1) labelled with 0.1% D-[U-13C] glucose. During the six hours following the glucose load, it was found that total glucose appearance was 0.97±0.04 g· kg·−1 and 1.2±0.04 g· kg·−1, exogenous glucose appearance was 0.51±0.02 g· kg·−1 and 0.84±0.04 g· kg·−1, endogenous glucose production was 0.44±0.04 g· kg·−1 and 0.35±0.06 g·kg·−1 after the 0.5 and 1 g·kg·−1 load respectively. These values are similar to those reported using glucose labelled with radioactive isotopes. These results show that reliable kinetic parameters of glucose metabolism can be determined, without health hazard, in humans, at low cost, using 13C labelled glucose analysed with a new gas chromatograph-isotope ratio mass spectrometer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00405104
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  • 10
    Electronic Resource
    Electronic Resource
    Dawn phenomenon in Type 1 (insulin-dependent) diabetic adolescents: influence of nocturnal growth hormone secretion (1988)
    Springer
    Diabetologia 31 (1988), S. 607-611 
    Details
    ISSN: 1432-0428
    Keywords: Dawn phenomenon ; Type 1 (insulin-dependent) diabetes ; adolescent ; growth hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In order to reassess the role of growth hormone in the dawn phenomenon, we studied eight C-peptide negative diabetic adolescents, who are likely to exhibit important nocturnal growth hormone surges. The insulin infusion rate necessary to maintain euglycaemia was predetermined in each patient from 22.00 hours to 01.00 hours, and then kept constant until 08.00 hours resulting in stable free insulin levels. Blood glucose rose from 4.3±0.7 mmol/l at 01.00 hours to 7.1±1.1 mmol/l at 08.00 hours (p〈0.01) secondary to an increased hepatic glucose production. All the subjects presented an important growth hormone secretion, ranging from 20 to 66 ng/ml (peak values) and from 3619 to 8621 ng·min· ml−1 (areas under the curve). The insulin infusion rate selected for each patient was positively correlated with the nocturnal growth hormone secretion (area under the curve) (r=0.87, p〈0.01). On the other hand, there was no relationship between the nocturnal growth hormone secretion and the magnitude of the early morning blood glucose rise (r=−0.48, p〉0.2). We conclude that, in Type 1 (insulin-dependent) diabetic adolescents, the dawn phenomenon exists but is moderate despite important growth hormone surges; the nocturnal growth hormone secretion influences the nocturnal insulin requirements but not the dawn phenomenon itself, if insulinisation is adequate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00264768
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