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  • 1
    Electronic Resource
    Electronic Resource
    Lipolysis in skeletal muscle is rapidly regulated by low physiological doses of insulin (1999)
    Springer
    Diabetologia 42 (1999), S. 1171-1174 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Skeletal muscle ; adipose tissue ; intramyocellular lipids ; lipolysis ; insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Both patients with Type II (non-insulin-dependent) diabetes mellitus and normoglycaemic, insulin resistant subjects were shown to have an increased lipid content in skeletal muscle, which correlates negatively with insulin sensitivity. Recently, it was shown that during a hyperinsulinaemic euglycaemic clamp interstitial glycerol was reduced not only in adipose tissue but also in skeletal muscle. To assess whether lipolysis of muscular lipids is also regulated by low physiological concentrations of insulin, we used the microdialysis technique in combination with a 3-step hyperinsulinaemic glucose clamp. Methods. Nineteen lean, healthy subjects (12 m/7 f) underwent a glucose clamp with various doses of insulin (GC I = 0.1, GC II = 0.25 and GC III = 1.0mU · kg–1· min–1). Two double lumen microdialysis catheters each were inserted in the paraumbilical subcutaneous adipose tissue and in skeletal muscle (tibialis anterior) to measure interstitial glycerol concentration (index of lipolysis) and ethanol outflow (index of tissue flow). Results. During the different steps of the glucose clamp, glycerol in adipose tissue was reduced to 81 ± 7 % (GC I), 55 ± 8 % (GC II) and 25 ± 5 % (GC III), respectively, of basal. In contrast, glycerol in skeletal muscle declined to 73 ± 5 % (GC I) and to 57 ± 6 % (GC II) but was not further reduced at GC III. Tissue flow was higher in the skeletal muscle and remained unchanged in both compartments throughout the experiment. Conclusion/interpretation. This study confirms the presence of glycerol release in skeletal muscle. Lipolysis in skeletal muscle and adipose tissue are suppressed similarly by minute and physiological increases in insulin but differently by supraphysiological increases. Inadequate suppression of intramuscular lipolysis resulting in increased availability of non-esterified fatty acids, could represent a potential mechanism involved in the pathogenesis of impaired glucose disposal, i. e. insulin resistance, in muscle. [Diabetologia (1999) 42: 1171–1174]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051288
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  • 2
    Electronic Resource
    Electronic Resource
    Characterisation of beta-cell dysfunction of impaired glucose tolerance: Evidence for impairment of incretin-induced insulin secretion (2000)
    Springer
    Diabetologia 43 (2000), S. 852-858 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type II diabetes, insulin resistance, GLP-1, arginine.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Our studies were undertaken to characterise the defective insulin secretion of impaired glucose tolerance (IGT).¶Methods. We studied 13 normal glucose tolerant subjects (NGT) and 12 subjects with IGT carefully matched for age, sex, BMI and waist-to-hip ratio. A modified hyperglycaemic clamp (10 mmol/l) with a standard 2-h square-wave hyperglycaemia, an additional glucagon-like-peptide (GLP)-1 phase (1.5 pmol · kg–1· min–1 over 80 min) and a final arginine bolus (5 g) was used to assess various phases of insulin secretion rate.¶Results. Insulin sensitivity during the second phase of the hyperglycaemic clamp was low in both groups but not significantly different (0.12 ± 0.021 in NGT vs 0.11 ± 0.013 μmol · kg–1· min–1· pmol–1 in IGT, p = 0.61). First-phase insulin secretion was lower in IGT (1467 ± 252 vs 3198 ± 527 pmol · min–1, p = 0.008) whereas the second phase was not (677 ± 61 vs 878 ± 117 pmol · min–1, p = 0.15). The acute insulin secretory peak in response to GLP-1 was absent in IGT subjects who only produced a late phase of GLP-1-induced insulin secretion rate which was lower (2228 ± 188 pmol · min–1) than in NGT subjects (3056 ± 327 pmol · min–1, p = 0.043). Insulin secretion in response to arginine was considerably although not significantly lower in IGT subjects. The relative impairment (per cent of the mean rate for NGT subjects) was greatest for the GLP-1 peak (19 ± 9 %).¶Conclusion/interpretation. In this Caucasian cohort a defective insulin secretion rate is essential for the development of IGT. The variable degrees of impairment of different phases of the insulin secretion rate indicate that several defects contribute to its abnormality in IGT. Defects in the incretin signalling pathway of the beta cell could contribute to the pathogenesis of beta-cell dysfunction of IGT and thus Type II (non-insulin-dependent) diabetes mellitus. [Diabetologia (2000) 43: 852–858]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051461
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  • 3
    Electronic Resource
    Electronic Resource
    Renal glucose production and utilization: new aspects in humans (1997)
    Springer
    Diabetologia 40 (1997), S. 749-757 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Endogenous glucose production ; gluconeogenesis ; glycogenolysis ; liver ; diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary According to current textbook wisdom the liver is the exclusive site of glucose production in humans in the postabsorptive state. Although many animal and in vitro data have documented that the kidney is capable of gluconeogenesis, production of glucose by the human kidney in the postabsorptive state has generally been regarded as negligible. This traditional view is based on net balance measurements which, other than after a prolonged fast or during metabolic acidosis, showed no significant net renal glucose release. However, recent studies have refuted this view by combining isotopic and balance techniques, which have demonstrated that renal glucose production accounts for 25 % of systemic glucose production. Moreover, these studies indicate that glucose production by the human kidney is stimulated by epinephrine, inhibited by insulin and is excessive in diabetes mellitus. Since renal glucose release is largely, if not exclusively, due to gluconeogenesis, it is likely that the kidney is as important a gluconeogenic organ as the liver. The most important renal gluconeogenic precursors appear to be lactate, glutamine and glycerol. The implications of these recent findings on the understanding of the physiology and pathophysiology of human glucose metabolism are discussed. [Diabetologia (1997) 40: 749–757].
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050745
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  • 4
    Electronic Resource
    Electronic Resource
    Stimulatory effect of increased non-esterified fatty acid concentrations on proinsulin processing in healthy humans (2000)
    Springer
    Diabetologia 43 (2000), S. 1368-1373 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin secretion, proinsulin secretion, non-esterified fatty acids, glucose, arginine.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. To assess the effect of increased concentrations of non-esterified fatty acids (NEFA) on proinsulin processing in healthy humans.¶Methods. We did a hyperglycaemic clamp (130 min duration, 8 mmol/l glucose, with a 5-g arginine bolus at min 120) before and after a 5-h infusion of Intralipid/heparin in 14 healthy subjects. Of the subjects eight underwent a saline control experiment. The proinsulin : insulin (PI:I) ratio immediately after the arginine bolus (122.5 to 125 min) was considered to provide an estimate for the conversion of proinsulin to insulin in the beta cell.¶Results. Concentrations of NEFA were 757 ± 86 μmol/l and 1669 ± 134 μmol/l (p 〈 0.001) after the 5-h infusion of saline or Intralipid, respectively. Insulin secretion rates were no different between the Intralipid and saline infusions (p = 0.73). There was no statistically significant difference for either the proinsulin concentration or the PI:I ratio during glucose stimulation alone (0 to 120 min). In response to arginine, in contrast, proinsulin remained unchanged during the saline infusion (from 31 ± 6 to 29 ± 7 pmol/l, p = 0.50) but decreased during 5 h of lipid infusion from (21 ± 3 to 15 ± 2 pmol/l, p = 0.02). The PI:I ratio in response to the arginine bolus was higher during the saline infusion (2.0 ± 0.2 % vs 1.7 ± 0.2 %, p = 0.04) but decreased during the Intralipid infusion (from 1.6 ± 0.2 % to 1.2 ± 0.1 %, p = 0.04).¶Conclusion/interpretation. The statistically significantly lower PI:I ratio in response to arginine during experimentally increased concentrations of NEFA suggests that NEFA increase the conversion of proinsulin to insulin in humans in vivo. [Diabetologia (2000) 43: 1368–1373]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051540
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  • 5
    Electronic Resource
    Electronic Resource
    Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans (1994)
    Springer
    Diabetologia 37 (1994), S. 697-702 
    Details
    ISSN: 1432-0428
    Keywords: Glycogen ; gluconeogenesis ; glycogenolysis ; hepatic glucose output
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relative contributions of gluconeogenesis and glycogenolysis to overall hepatic glucose output in postabsorptive normal humans and those of the indirect and direct pathways for glycogen synthesis, we studied six normal volunteers, who had been fasted for 16 h to reduce their hepatic glycogen stores, and then ingested glucose (250 g over 10 h) enriched with [6-3H] glucose to replenish and label their hepatic glycogen. After a 10-h overnight fast, release of the [6-3H] glucose into the circulation was traced with [2-3H] glucose to estimate breakdown of glycogen that had been formed via the direct pathway while gluconeogenesis was simultaneously estimated by incorporation of infused [14C] lactate into plasma glucose. We found that release of [6-3H] glucose into plasma (6.79±0.69 μmol · kg−1 · min−1) accounted for 46±5% of hepatic glucose output (15.0±0.7 μmol · kg−1· min−1) while glucose formed from lactate (2.71±0.28 μmol · kg−1 · min−1) accounted for 19±2% of hepatic glucose output. Since these determinations underestimate direct pathway glycogenolysis and overall gluconeogenesis, a maximal estimate for the contribution of indirect pathway glycogenolysis to hepatic glucose output is obtained by subtracting the sum of direct pathway glycogenolysis and lactate gluconeogenesis from hepatic glucose output. This amounted to a maximum of 36±5 % of hepatic glucose output and 44±6% of overall glycogenolysis. Assuming that the relative proportions of direct and indirect pathway glycogen breakdown would reflect the relative contributions of these pathways to glycogen formation, we conclude that under our experimental conditions the direct pathway is the predominant route for glycogen formation in man and that in overnight fasted humans, hepatic glucose output is mainly the result of glycogenolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417694
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  • 6
    Electronic Resource
    Electronic Resource
    Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans (1994)
    Springer
    Diabetologia 37 (1994), S. 697-702 
    Details
    ISSN: 1432-0428
    Keywords: Key words Glycogen, gluconeogenesis, glycogenolysis, hepatic glucose output.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relative contributions of gluconeogenesis and glycogenolysis to overall hepatic glucose output in postabsorptive normal humans and those of the indirect and direct pathways for glycogen synthesis, we studied six normal volunteers, who had been fasted for 16 h to reduce their hepatic glycogen stores, and then ingested glucose (250 g over 10 h) enriched with [6-3H] glucose to replenish and label their hepatic glycogen. After a 10-h overnight fast, release of the [6-3H] glucose into the circulation was traced with [2-3H] glucose to estimate breakdown of glycogen that had been formed via the direct pathway while gluconeogenesis was simultaneously estimated by incorporation of infused [14C] lactate into plasma glucose. We found that release of [6-3H] glucose into plasma (6.79±0.69 µmol·kg−1·min−1) accounted for 46±5 % of hepatic glucose output (15.0±0.7 µmol·kg−1· min−1) while glucose formed from lactate (2.71± 0.28 µmol·kg−1·min−1) accounted for 19±2 % of hepatic glucose output. Since these determinations underestimate direct pathway glycogenolysis and overall gluconeogenesis, a maximal estimate for the contribution of indirect pathway glycogenolysis to hepatic glucose output is obtained by subtracting the sum of direct pathway glycogenolysis and lactate gluconeogenesis from hepatic glucose output. This amounted to a maximum of 36±5 % of hepatic glucose output and 44±6 % of overall glycogenolysis. Assuming that the relative proportions of direct and indirect pathway glycogen breakdown would reflect the relative contributions of these pathways to glycogen formation, we conclude that under our experimental conditions the direct pathway is the predominant route for glycogen formation in man and that in overnight fasted humans, hepatic glucose output is mainly the result of glycogenolysis. [Diabetologia (1994) 37: 697–702]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417694
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  • 7
    Electronic Resource
    Electronic Resource
    Systemic vasculitis positive for circulating anti-neutrophil cytoplasmic antibodies and with predominantly neurological presentation (1993)
    Springer
    Journal of molecular medicine 71 (1993), S. 613-615 
    Details
    ISSN: 1432-1440
    Keywords: C-ANCA ; Wegener granulomatosis ; Cerebral vasculitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 57-year-old male patient suffering from dramatically deteriorating diffuse and focal central nervous system symptoms was admitted to hospital after a short prodromal period in a somnolent state. He was diagnosed as having systemic vasculitis positive for circulating anti-neutrophil cytoplasmic antibodies, primarily involving the brain, but also most other organ systems. Circulating anti-neutrophil cytoplasmic antibodies are highly specific for Wegener granulomatosis, though they have been detected in rare cases of other vasculitic syndromes. Central nervous system lesions as presenting signs in Wegener granulomatosis have to be regarded as rare. This case nonetheless suggests that Wegener granulomatosis has to be considered in patients with a predominantly cerebral manifestation of a vasculitic syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00184485
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  • 8
    Electronic Resource
    Electronic Resource
    Intensive insulin therapy combined with metformin in obese type 2 diabetec patients (2000)
    Springer
    Acta diabetologica 37 (2000), S. 13-18 
    Details
    ISSN: 1432-5233
    Keywords: Key words NIDDM ; Biguanides ; Combination therapy ; Insulin treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Unlike other pharmacological therapies used in obese type 2 diabetic patients, metformin has been shown to improve glycemic control with lower insulin levels and not to involve weight gain. We therefore examined the effect of adjunct metformin in 13 severely obese type 2 diabetic patients (BMI 39.3 ± 3.9 kg/m2) in suboptimal glycemic control pretreated with intensified insulin therapy. Patients were randomly assigned to either metformin or placebo treatment (double-blind) for 10 weeks and after a 2 week washout period received the opposite treatment, respectively, for 10 additional weeks. HbA1c decreased comparably during placebo (from 8.1 ± 0.4 to 7.6 ± 0.3%) and metformin (from 8.5 ± 0.4 to 7.4 ± 0.3%, p = 0.29 vs. placebo). Changes in fasting glucose levels were also not different between placebo (from 9.3 ± 0.7 to 9.5 ± 0.7 mM) and metformin (from 10.3 ± 0.5 to 9.5 ± 0.6 mM, p = 0.44 vs. placebo) Total exogenous insulin requirements decreased from 53 ± 10 to 35 ± 7 units during metformin treatment (p = 0.11). Metformin had no effect on body weight and serum triglycerides but marginally decreased serum cholesterol levels (from 239 ± 18 to 211 ± 14 mg/dl, p = 0.005, p = 0.08 vs. placebo). During the oral glucose tolerance test no differences were observed in the areas under the curve for glucose and insulin while that for C-peptide showed a tendency to increase during metformin administration. We conclude that addition of metformin to insulin treatment in severely obese type 2 diabetic patient improves glycemia but no hyperinsulinemia in comparison to intensive insulin therapy alone. With adjunct metformin, ∼30% less exogenous insulin is required. With respect to glycemia and lipids, adjunct metformin can be a reasonable treatment alternative in selective obese patients with type 2 diabetes already on intensive insulin therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920070030
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