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  • Electronic Resource  (5)
  • indirect calorimetry  (2)
  • ketogenesis  (2)
  • Arbuscular mycorrhiza  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Biochemical approaches to the study of plant-fungal interactions in arbuscular mycorrhiza (1994)
    Springer
    Cellular and molecular life sciences 50 (1994), S. 919-925 
    Details
    ISSN: 1420-9071
    Keywords: Arbuscular mycorrhiza ; abscisic acid ; carotenoid ; Glomus ; nitrate reductase ; mycorradicin ; sterols ; yellow pigment in mycorrhiza
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract This communication compares some biochemical methods for quantifying colonization by arbuscular mycorrhizal (AM) fungi. The degree of mycorrhizal colonization can conveniently be measured by determining fungal specific sterols. AM-colonized plants show a specific synthesis of 24-methylene cholesterol and an enhanced level of campesterol (=24-methyl cholesterol). A gene probe for nitrate reductase, the key enzyme for nitrogen assimilation, has been developed, which allows the monitoring of the distribution of this enzyme in fungi. Among the phytohormones tested, only abscisic acid (ABA) is found at a considerably higher level in AM-colonized plants than in controls. The concentration of ABA is about twenty times higher in spores and hyphae of the AM fungusGlomus than in maize roots. Other phytohormones (auxins, cytokinins) do not show such alterations after mycorrhizal colonization. The roots of gramineous plants become yellow as a result of mycorrhizal colonization. The yellow pigment(s) formed is (are) deposited in larger quantities in the vacuole(s) of the root parenchyma and endodermis cells during the development of the gramineous plants. A substance isolated from such roots has now been identified as a C-14 carotenoid with two carboxylic groups, and named mycorradicin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923479
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  • 2
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse (1996)
    Springer
    Diabetologia 39 (1996), S. 961-969 
    Details
    ISSN: 1432-0428
    Keywords: Substrate oxidation ; energy expenditure ; lipolysis ; ketogenesis ; “dawn” phenomenon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27±4 years, BMI 21.8±1.7 kg/m2) were treated with NaCl 0.9% (saline) or IGF-I (8 Μg · kg−1 · h−1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg−1 · day−1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80% (p〈0.02) and C-peptide levels by 78% (p〈0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10±0.43 (saline) to 2.79±0.37 ml · 100ml−1 · min−1 (IGF-I) (p〈0.02). GH-pulse: 10 h after i.v. GH injection serum GH peaked at 40.9±7.4 ng/ml. GH did not influence circulating levels of total IGFI, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702±267 (saline) and 885±236 (IGF-I) to 963±215 (saline) (p〈0.05) and 1815±586 Μmol/l (IGF-I) (p〈0.02), respectively; after 5 h, 3-OH-butyrate rose from 242±234 (saline) and 340±280 (IGF-I) to 678±638 (saline) (p〈0.02) and 1115±578 Μmol/l (IGF-I) (p〈0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44±195 to 300±370 after 20 min (p〈0.03) and to 287±91 nmol · 100 ml−1 · min−1after 120 min (p〈0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403916
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  • 3
    Electronic Resource
    Electronic Resource
    Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse (1996)
    Springer
    Diabetologia 39 (1996), S. 961-969 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Substrate oxidation ; energy expenditure ; lipolysis ; ketogenesis ; “dawn” phenomenon.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27 ± 4 years, BMI 21.8 ± 1.7 kg/m2) were treated with NaCl 0.9 % (saline) or IGF-I (8 μg · kg–1· h–1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg–1· day–1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80 % (p 〈 0.02) and C-peptide levels by 78 % (p 〈 0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10 ± 0.43 (saline) to 2.79 ± 0.37 ml · 100ml–1· min–1 (IGF-I) (p 〈 0.02). GH-pulse: 10 h after i. v. GH injection serum GH peaked at 40.9 ± 7.4 ng/ml. GH did not influence circulating levels of total IGF-I, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702 ± 267 (saline) and 885 ± 236 (IGF-I) to 963 ± 215 (saline) (p 〈 0.05) and 1815 ± 586 μmol/l (IGF-I) (p 〈 0.02), respectively; after 5 h, 3-OH-butyrate rose from 242 ± 234 (saline) and 340 ± 280 (IGF-I) to 678 ± 638 (saline) (p 〈 0.02) and 1115 ± 578 μmol/l (IGF-I) (p 〈 0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44 ± 195 to 300 ± 370 after 20 min (p 〈 0.03) and to 287 ± 91 nmol · 100 ml–1· min–1after 120 min (p 〈 0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased. [Diabetologia (1996) 39: 961–969]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403916
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  • 4
    Electronic Resource
    Electronic Resource
    Basal and insulin stimulated substrate metabolism in tumour induced hypoglycaemia; evidence for increased muscle glucose uptake (1991)
    Springer
    Diabetologia 34 (1991), S. 17-20 
    Details
    ISSN: 1432-0428
    Keywords: Glucose turnover ; forearm technique ; intermediary metabolites ; euglycaemic and hypoglycaemic glucose clamp ; indirect calorimetry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary While it has very recently been reported that tumour induced hypoglycaemia is characterised by elevated production of insulin-like growth factor 2, the tissues responsible for induction of hypoglycaemia are largely unknown. We have investigated a patient with a large retroperitoneal mass and spontaneous hypoglycaemia. When compared to a reference population the patient displayed: (1) An increased glucose disposal rate and a five-fold elevation of forearm glucose uptake. (2) A decreased endogenous glucose production rate. (3) Decreased circulating levels of lipid intermediates. (4) Increased glucose oxidation and decreased lipid oxidation. (5) Low circulating levels of insulin-like growth factor 2 and insulin-like growth factor-binding protein-3 and normal levels of insulin-like growth factor 1. (6) Normal insulin sensitivity (euglycaemic glucose clamp). Blood concentrations of insulin, C-peptide, proinsulin, glucagon, growth hormone and catecholamines were within normal range, but the growth hormone response to hypoglycaemia was blunted. The data suggest that the mechanisms behind tumour induced hypoglycaemia are of systemic nature and that the tissue most prominently affected is striated muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404019
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  • 5
    Electronic Resource
    Electronic Resource
    In vivo insulin action and muscle glycogen synthase activity in Type 2 (non-insulin-dependent) diabetes mellitus: effects of diet treatment (1992)
    Springer
    Diabetologia 35 (1992), S. 777-784 
    Details
    ISSN: 1432-0428
    Keywords: Insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus ; hyperinsulinaemic clamp ; indirect calorimetry ; forearm glucose uptake ; muscle ; glycogen synthase ; insulin receptor kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin resistant glucose metabolism is a key element in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus. Insulin resistance may be of both primary (genetic) and secondary (metabolic) origin. Before and after diet-induced improvement of glycaemic control seven obese patients with newly-diagnosed Type 2 diabetes were studied with the euglycaemic clamp technique in combination with indirect calorimetry and forearm glucose balance. Muscle biopsies were obtained in the basal state and again after 3 h of hyperinsulinaemia (200 mU/l) for studies of insulin receptor and glycogen synthase activities. Similar studies were performed in seven matched control subjects. Insulin-stimulated glucose utilization improved from 110±11 to 183±23 mg·m−2·min−1 (p〈0.03); control subjects: 219+23 mg·m−2·min−1 (p=NS, vs post-diet Type 2 diabetes). Nonoxidative glucose disposal increased from 74±17 to 138+19 mg·m−2·min−1 (p〈0.03), control subjects: 159±22 mg· m−2·m−1 (p=NS, vs post-diet Type 2 diabetic patients). Forearm blood glucose uptake during hyperinsulinaemia increased from 1.58±0.54 to 3.35±0.23 μmol·l−1·min−1 (p〈0.05), control subjects: 2.99±0.86 μmol·l−1·min−1 (p=NS, vs post-diet Type 2 diabetes). After diet therapy the increase in insulin sensitivity correlated with reductions in fasting plasma glucose levels (r=0.97, p〈0.001), reductions in serum fructosamine (r=0.77, p〈0.05), and weight loss (r=0.78, p〈0.05). Values of muscle glycogen synthase sensitivity to glucose 6-phosphate (A0.5 for glucose 6-phosphate) were similar in the basal state. However, insulin stimulation of glycogen synthase was more pronounced after diet treatment (A0.5: 0.43±0.06 (before) vs 0.30±0.04 mmol/l (after); p〈0.03; control subjects: 0.22±0.03 mmol/l). Muscle insulin receptor binding and kinase activity were similar before and after diet treatment and comparable to values in the control group. The data suggest that impaired insulin stimulation of in vivo glucose turn-over and muscle glycogen synthase activity tend to be restored during successful diet treatment of patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429100
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