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  • 1
    Electronic Resource
    Electronic Resource
    Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1202-1208 
    Details
    ISSN: 1432-0428
    Keywords: Intracerebroventricular (i.c.v.) ; neuropeptide Y (NPY) ; food intake ; body weight gain ; in vivo glucose uptake ; muscle insulin resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four- and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-d-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebro-ventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399793
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  • 2
    Electronic Resource
    Electronic Resource
    Induction and reversibility of an obesity syndrome by intracerebroventricular neuropeptide Y administration to normal rats (1994)
    Springer
    Diabetologia 37 (1994), S. 1202-1208 
    Details
    ISSN: 1432-0428
    Keywords: Key words Intracerebroventricular (i. c. v.) ; neuropeptide Y (NPY) ; food intake ; body weight gain ; in vivo glucose uptake ; muscle insulin resistance.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricular neuropeptide Y (NPY) administration to normal rats for 7 days produced a sustained, threefold increase in food intake, resulting in a body weight gain of more than 40 g. Basal plasma insulin and triglyceride levels were increased in NPY-treated compared to vehicle-infused rats by about four- and two-fold, respectively. The glucose utilization index of white adipose tissue, measured by the labelled 2-deoxy-d-glucose technique was four times higher in NPY-treated rats compared to controls. This change was accompanied by an increase in the insulin responsive glucose transporter protein (GLUT 4). In marked contrast, muscle glucose utilization was decreased in NPY-treated compared to vehicle-infused animals. This change was accompanied by an increase in triglyceride content. When NPY-treated rats were prevented from overeating, there was no decrease in muscle glucose uptake, nor was there an increase in muscle triglyceride content. This suggests that muscle insulin resistance of ad libitum-fed NPY-treated rats is due to a glucose-fatty acid (Randle) cycle. When intracerebroventricular NPY administration was stopped and rats kept without any treatment for 7 additional days, all the abnormalities brought about by the neuropeptide were normalized. A tonic central effect of NPY is therefore needed to elicit and maintain most of the hormonal and metabolic abnormalities observed in the present study. Such abnormalities are analogous to those seen in the dynamic phase of obesity syndromes in which high hypothalamic NPY levels have been reported. [Diabetologia (1994) 37: 1202–1208]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399793
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of intravenous neuropeptide Y on insulin secretion and insulin sensitivity in skeletal muscle in normal rats (1998)
    Springer
    Diabetologia 41 (1998), S. 1361-1367 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Neuropeptide Y ; insulin secretion ; insulin sensitivity ; leptin ; clamp technique ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intracerebroventricular administration of neuropeptide Y to normal rats induces a syndrome characterised by obesity, hyperinsulinaemia, insulin resistance and over expression of the adipose tissue ob gene. Little is known about the effect of circulating neuropeptide Y on glucose metabolism, insulin secretion and leptin. We therefore aimed to evaluate the effect of an intravenous infusion of neuropeptide Y on glucose disposal, endogenous glucose production, whole body glycolytic flux, and glucose storage as assessed during euglycaemic hyperinsulinaemic clamp. In addition, the insulin-stimulated glucose utilisation index in individual tissues was measured by the 2-deoxy-[1-3H]-glucose technique. The effect of neuropeptide Y on insulin secretion was evaluated by hyperglycaemic clamp. Infusion did not induce any change in endogenous glucose production during basal conditions or at the end of the clamp. Glucose disposal was significantly increased in the rats given neuropeptide Y compared with controls (27.8 ± 1.3 vs 24.3 ± 1.6 mg · min–1· kg–1; p 〈 0.05) as was the glycolytic flux (18.9 ± 1.6 vs 14.4 ± 0.8 mg · min–1· kg–1; p 〈 0.05), while glucose storage was comparable in the two groups. In skeletal muscle, the glucose utilisation index was increased significantly in rats given neuropeptide Y. The glucose utilisation index in subcutaneous and epididimal adipose tissue was not significantly different between the two groups. Plasma leptin was significantly increased by hyperinsulinaemia, but was not affected by neuropeptide Y infusion. Both the early and late phase of the insulin response to hyperglycaemia were significantly reduced by neuropeptide Y. In conclusion neuropeptide Y infusion may increase insulin-induced glucose disposal in normal rats, accelerating its utilisation through the glycolytic pathway. Neuropeptide Y reduces both phases of the insulin response to hyperglycaemia. [Diabetologia (1998) 41: 1361–1367]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051077
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Review article: adipocytokines and insulin resistance (2005)
    Oxford, UK : Blackwell Publishing Ltd
    Alimentary pharmacology & therapeutics 22 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Insulin resistance has been implicated as one possible factor that links visceral obesity to unfavourable metabolic and cardiovascular consequences. However, the mechanism whereby adipose tissue causes alterations in insulin action remains unclear. White adipose tissue is secreting several hormones, particularly leptin and adiponectin, and a variety of other protein signals: the adipocytokines. They include proteins involved in the regulation of energy balance, lipid and glucose metabolism as well as angiogenesis, vascular and blood pressure regulation. Visceral obesity and inflammation within white adipose tissue may be a crucial step contributing to the emergence of insulin resistance, type 2 diabetes and atherosclerosis. A growing list of adipocytokines involved in inflammation (IL-1β, IL-6, IL-8, IL-10, TNF-α, TGF-β,) and the acute-phase response (serum amyloid A, PAI-1) have been found to be increased in the metabolic syndrome. It is, however, unclear as to the extent adipose tissue contributes quantitatively to the elevated circulating levels of these factors in obesity and how they may affect the insulin-dependent tissues. This review describes the role of the currently known adipocytokines and hormones released by adipose tissue in generating the insulin resistance state and the chronic inflammatory profile which frequently goes together with visceral obesity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2005.02587.x
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Effect of exercise on plasma kallikrein and muscular phospholipase A"2 activity in rats
    Amsterdam : Elsevier
    Molecular and Cellular Endocrinology 45 (1986), S. 65-70 
    Details
    ISSN: 0303-7207
    Keywords: exercise ; kallikrein ; muscular glucose uptake ; muscular phospholipase A"2
    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)90083-3
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  • 6
    Electronic Resource
    Electronic Resource
    Role of antecedent mumps and reovirus infections on the development of type 1 (insuling-dependent) diabetes (1985)
    Springer
    European journal of epidemiology 1 (1985), S. 172-179 
    Details
    ISSN: 1573-7284
    Keywords: Diabetes ; Reovirus ; Mumps ; Measles ; Viral antibodies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Type 1 diabetes mellitus is thought to derive from organ-specific autoimmune reactions, probably triggered by environmental factors. In view of the possible involvement of mumps virus and reoviruses in the pathogenesis of autoimmune endocrine disease, serum antibody levels to these viruses were measured in newly-diagnosed diabetic patients aged 5 to 25 years and in matched control subjects. Diabetic patients showed a significantly lower prevalence and reduced titers of antibodies to mumps and reoviruses. By contrast, the antibody response to measles virus (a non-diabetogenic agent) was remarkably similar in the two groups. It is suggested that individuals with an impaired humoral response to some viral agents are at increased risk of developing diabetes when exposed to pancreotropic viruses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00234091
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  • 7
    Electronic Resource
    Electronic Resource
    Impaired counterregulatory hormonal and metabolic response to exhaustive exercise in obese subjects (1997)
    Springer
    Acta diabetologica 34 (1997), S. 61-66 
    Details
    ISSN: 1432-5233
    Keywords: Key words Exercise ; Obesity ; Counterregulatory hormones ; Insulin resistance ; Energy expenditure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A reduction of postprandial thermogenesis has been described in obesity; insulin resistance and/or decreased sympathetic nervous system activity seem to play the major role in its pathogenesis. On the other hand, a normal energy expenditure during exercise has been reported. At present, the response and the role of catecholamines in energy metabolism during exercise in obesity have not been well clarified yet. The aim of this work was to study the metabolic and hormonal changes caused by intense exercise in obesity. Nine obese subjects and ten normal weight controls were submitted to exhaustive exercise on a cycloergometer. Blood glucose, free fatty acids (FFA), glycerol, lactate, β-OH-butyrate, insulin, glucagon, plasma growth hormone (HGH), catecholamine plasma levels were assayed before and at the end of exercise, and after a recovery period. The energy cost of exercise was evaluated by indirect calorimetry. In our experiment muscular exercise did not provoke any change in blood glucose and FFA plasma levels in either of our groups. In the obese subjects the insulin plasma levels were higher than in the controls. Glucagon plasma levels did not change. The exercise responses of norepinephrine (NE) (4.28±0.74 vs 8.81±1.35 nmol/l; P〈0.01), epinephrine (E) (234.21±64.18 vs 560.51±83.38 pmol/l; P〈0.01) and plasma growth hormone (HGH) (134.84±58.97 vs 825.92±195.25 pmol/l; P〈0.01) were significantly lower in obese subjects. At the end of exercise, the thermic effect of exercise did not differ between obese and control subjects (0.335±0.038 vs 0.425±0.040 kJ/min×kg fat-free mass. Our findings indicate that an impaired counterregulatory hormone response to exercise exists in obese subjects. The thermic effect of exercise does not seem to be affected by either the reduced catecholamine response nor insulin resistance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920050068
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