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  • 1
    Electronic Resource
    Electronic Resource
    Therapeutic Perspectives for Melatonin Agonists and Antagonists (2003)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Melatonin is a neurohormone synthesized in the pineal gland during the dark period in all species, including humans. The diversity and differences in melatonin receptor distribution in the brain and extracerebral organs suggest multiple functional roles for melatonin. Administration of melatonin agonists reduces neophobia and treatment with a melatonin antagonist during the dark period reverses the anxiolytic-like effect of endogenous melatonin. Chronic treatment with agonists prevents various perturbations induced by chronic mild stress. Melatonin in vivo directly constricts cerebral arterioles in rats and decreases the lower limit of cerebral blood flow autoregulation, suggesting that melatonin may diminish the risk of hypoperfusion-induced cerebral ischemia. At the extracerebral level, melatonin regulates intestinal motility in rats. The intestinal postprandial motor response is shorter in the dark phase than in the light phase and this reduction is reversed in animals pretreated with a melatonin antagonist. Moreover, melatonin reduces the duration of cholecystokinin excitomotor effect. Endogenous melatonin may modulate intestinal motility to coordinate intestinal functions such as digestion and transit and control the metabolism of the animal. An adipocyte melatonin binding site may also participate in this control. Melatonin is involved in a wide range of physiological functions. The question remains as to whether evolution, adaptation and diurnal life have modified the physiological role of melatonin in humans. Moreover, the functional role of each of the receptor subtypes has to be characterized to design selective ligands to treat specific diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2003.01016.x
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  • 2
    Electronic Resource
    Electronic Resource
    Cerebral Insulin Increases Brain Response to Glucose (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The hypothalamus participates in the regulation of carbohydrate metabolism involving a feedback loop between the brain and the periphery in which glucose-sensitive hypothalamic areas appear to be involved. We have previously shown that a glucose injection (9 mg/kg) in the carotid artery toward the brain, in an amount that did not modify glycaemia, caused a rapid and transient increase in plasma insulin concentrations. To determine whether central insulin could influence this response, we investigated the change in central glucose-induced insulin secretion in intracerebroventricular (i.c.v) insulin-injected rats and in hyperinsulinaemic obese Zucker rats. Central glucose-induced insulin secretion was increased by 50% in i.c.v. insulin-injected rats compared to control rats. When a similar test was performed at a lower dose of glucose (3 mg/kg), a significant insulin secretion was observed only in rats submitted to a prior central insulin injection. These data indicate an increase in the brain response to glucose after insulin treatment. Using an identical lower glucose dose, we also demonstrated an enhanced brain glucose sensitivity in hyperinsulinaemic and insulin-resistant obese Zucker rats. Together, these results indicate that acute i.c.v. insulin or pathological hyperinsulinaemic state (i.e. obese Zucker rat) modulates the nervous control of insulin secretion by increasing the brain response to glucose.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2003.00961.x
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  • 3
    Electronic Resource
    Electronic Resource
    Acute Intracarotid Glucose Injection Towards the Brain Induces Specific c-fos Activation in Hypothalamic Nuclei: Involvement of Astrocytes in Cerebral Glucose-Sensing in Rats (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 16 (2004), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The detection of changes in glucose level constitutes the first step of the control of glucose homeostasis. Glucose sensors are therefore expected to be present in different parts of the body and particularly in the central nervous system. Some studies have already attempted to determine glucose-sensitive cerebral structures either after a glucoprivic stimulus or after prolonged hyperglycaemia. By analogy to beta cells, it was postulated that the glucose sensors in the brain could involve GLUT2, glucokinase and/or ATP-sensitive K+ channels. Surprisingly, GLUT2 was mainly found in astrocytes. Thus, the aims of the present investigation were to determine, in awake rats: (i) the hypothalamic areas that respond to acute hyperglycaemic condition induced by an intracarotid injection of glucose and (ii) the involvement of astrocytes in glucose-sensing by the use of a glial drug, methionine sulfoximine. Rats were given intracarotid injections of glucose solution to trigger a transient insulin secretion without change in peripheral glycaemia, thus involving only central nervous regulation. Hypothalamic activation was determined by immunodetection of the immediate early gene c-fos protein. Acute glucose injection induces significant activation of arcuate and paraventricular nuclei. This stimulation mainly affects neurones in both nuclei, but also astrocytes in the former as illustrated by double immunohistochemistry (Fos and neuronal nuclei or glial fibrillary acidic protein). After specific impairment of astrocyte metabolism by methionine sulfoximine, cerebral activation disappears in the arcuate nucleus, correlated with the lack of cerebral glucose-induced insulin secretion. Therefore, arcuate and paraventricular hypothalamic nuclei are able to detect acute cerebral hyperglycaemia, leading to a peripheral stimulation of insulin secretion. Arcuate nucleus and more especially astrocytes in this nucleus play a pivotal role in glucose-sensing.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.2004.01185.x
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  • 4
    Electronic Resource
    Electronic Resource
    Fiber type composition and enzyme activities of muscles in two models of obese rats
    Amsterdam : Elsevier
    Comparative Biochemistry and Physiology -- Part B: Biochemistry and 106 (1993), S. 269-272 
    Details
    ISSN: 0305-0491
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0305-0491(93)90299-K
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  • 5
    Electronic Resource
    Electronic Resource
    Changes in islet blood flow in rats with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 677-680 
    Details
    ISSN: 1432-0428
    Keywords: GK rats ; n0-STZ ; insulin ; islet blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet blood flow was quantified in NIDDM rats either of the GK strain on after neonatal injection of STZ (n0-STZ), using the non-radioactive microsphere technique. In the basal state, there was a good correlation between plasma insulin level and islet blood flow, i.e. both were increased or decreased in comparison to those of control rats in GK and n0-STZ rats, respectively. The increased islet blood flow and plasma insulin levels observed in the GK rats were abolished by bilateral subdiaphragmatic vagotomy. During a glucose challenge, whereas plasma insulin and islet blood flow were doubled in control rats, these parameters were not modified in the diabetic rats. These data demonstrate an alteration in the islet blood flow of diabetic rats during a glucose challenge which could participate in the abnormal glucose-induced insulin secretion previously described in these two models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417691
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  • 6
    Electronic Resource
    Electronic Resource
    Normal insulin sensitivity during the phase of glucose intolerance but insulin resistance at the onset of diabetes in the spontaneously diabetic BB rat (1989)
    Springer
    Diabetologia 32 (1989), S. 839-844 
    Details
    ISSN: 1432-0428
    Keywords: BB rat ; diabetes ; glucose intolerance ; insulin sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In diabetes-prone BB rats, 30 to 50% of animals undergo autoimmune destruction of the pancreatic B-cells leading to a short period of glucose intolerance, followed by an abrupt onset of diabetes. We have examined whether the glucose intolerance period and the onset of diabetes are associated with changes in insulin sensitivity, using the euglycaemic hyperinsulinaemic clamp coupled with [3-3H] glucose infusion. Glucose intolerant rats were detected by a transient glycosuria one hour after an oral glucose load performed every four days. Insulin sensitivity studied in these rats the day following their detection was normal. Other diabetes-prone BB rats were tested daily and studied on the first day of glycosuria. In the basal state, glucose production was increased in diabetic rats (11.3±1.1 vs 7.1±0.8mg·min−1·kg−1, p〈0.05). Tissue glucose utilization was similar in diabetic and control rats (8.3±0.5 vs 7.1±0.8mg·min−1·kg−1) despite a three fold higher glycaemia in the diabetic rats. During the hyperinsulinaemic clamps, glycaemia was clamped at 6.1–6.6 mmol/l in diabetic and control rats. A decreased insulin sensitivity was observed in diabetic rats at submaximal (200 μU/ml) and maximal (1500 μU/ml) insulin concentrations for both inhibition of hepatic glucose production and stimulation of glucose utilization. No autoantibodies against insulin could be detected in the plasma of diabetic rats. Plasma concentrations of glucagon, catecholamines, ketone bodies and fatty acids were similar in control and diabetic rats during the clamp studies. Our results suggest that the decrease of basal insulin concentration is responsible for the insulin resistance in the diabetic BB rat at onset of diabetes, either directly or through the increased glycaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00297448
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  • 7
    Electronic Resource
    Electronic Resource
    Increased mitogen-activated protein kinase expression and activity in white adipose tissue of ventromedial hypothalamus-lesioned rats (1997)
    Springer
    Diabetologia 40 (1997), S. 533-540 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin signalling ; MAP-kinase ; insulin receptor ; insulin sensitivity ; obesity ; white adipose tissue.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ventromedial hypothalamus lesions in rats induce hyperphagia and hyperinsulinaemia associated with a rapid growth of white adipose tissue resulting in massive obesity. It has been shown previously that at an early stage after the lesion, during the dynamic phase of obesity, the white adipose tissue is hyper-responsive to insulin. In the present work, we show that the effects of insulin on the autophosphorylation of the insulin receptor and on its tyrosine-kinase activity towards endogenous substrates are similar in intact adipocytes of control and ventromedial hypothalamus lesioned rats. One week after the lesion, the expression of phosphatidylinisitol 3-kinase and RAF-1 kinase, evaluated by Western-blotting, was similar in control and ventromedial hypothalamus lesioned rats. In contrast, an important increase in the expression of extracellular signal regulated kinase 1 protein was observed in white adipose tissue of ventromedial hypothalamus lesioned compared to control animals. No difference in the expression of extracellular signal regulated kinase 1 mRNA was observed in adipose tissue of control and ventromedial hypothalamus lesioned rats, suggesting that a post-transcriptional mechanism is involved in the over-expression of extracellular signal regulated kinase 1. The kinase activity of extracellular signal regulated kinase 1 and 2 is also markedly increased in adipocytes of ventromedial hypothalamus lesioned compared to control rats, both in the basal state and after insulin stimulation. Six weeks after the ventromedial hypothalamus lesion, this increase in mitogen-activated protein kinase expression and activity was still observed in adipocytes of ventromedial hypothalamus lesioned rats. These results suggest that an early and sustained increase in the expression and activity of mitogen-activated protein kinase may participate in the development of white adipose tissue in ventromedial hypothalamus lesioned rats. [Diabetologia (1997) 40: 533–540]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050712
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  • 8
    Electronic Resource
    Electronic Resource
    In vivo and in vitro increased pancreatic beta-cell sensitivity to glucose in normal rats submitted to a 48-h hyperglycaemic period (1993)
    Springer
    Diabetologia 36 (1993), S. 589-595 
    Details
    ISSN: 1432-0428
    Keywords: Glucose infusion ; in vivo insulin secretion ; in vitro insulin secretion ; beta-cell sensitivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the importance of the level and the duration of glucose stimulation on the in vivo and in vitro insulin response to glucose in normal rats previously submitted to hyperglycaemia. Rats were made hyperglycaemic by a 48-h glucose infusion. Glucose-induced insulin secretion was investigated in vivo by a 20-min hyperglycaemic clamp and in vitro by the isolated perfused pancreas technique, 3 h after the end of the in vivo glucose infusion. In glucose-infused rats, as compared to controls, in vivo incremental plasma insulin values above baseline integrated over the 20-min hyperglycaemic clamp (ΔI) were five times higher during 8 mmol/l glucose clamp, only two times higher in 11 mmol/l glucose clamp and no different in 16.5 mmol/l. Compared to the controls, in vitro incremental plasma insulin concentration above baseline integrated over a 20-min period (ΔI) in glucose-infused rats was 16 times higher in response to 2.8 mmol/l glucose, two times higher in response to 5.5 mmol/l, similar in response to 8.3 mmol/l and significantly lower in response to 16.5 mmol/l. In conclusion, our data suggest that a 48-h hyperglycaemic period results in an increased response of the pancreatic beta cell to low glucose. The response is immediately maximal and can not be increased with higher glucose concentrations. This situation could explain the apparent minimal effect of high concentrations on in vitro insulin secretion in previously hyperglycaemic rats and may provide insights into the sequence of events leading to the impairment of beta-cell function in Type 2 (non-insulin-dependent) diabetes mellitus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404066
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  • 9
    Electronic Resource
    Electronic Resource
    Changes in islet blood flow in rats with NIDDM (1994)
    Springer
    Diabetologia 37 (1994), S. 677-680 
    Details
    ISSN: 1432-0428
    Keywords: Key words GK rats, n0-STZ, insulin, islet blood flow.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet blood flow was quantified in NIDDM rats either of the GK strain on after neonatal injection of STZ (n0-STZ), using the non-radioactive microsphere technique. In the basal state, there was a good correlation between plasma insulin level and islet blood flow, i. e. both were increased or decreased in comparison to those of control rats in GK and n0-STZ rats, respectively. The increased islet blood flow and plasma insulin levels observed in the GK rats were abolished by bilateral subdiaphragmatic vagotomy. During a glucose challenge, whereas plasma insulin and islet blood flow were doubled in control rats, these parameters were not modified in the diabetic rats. These data demonstrate an alteration in the islet blood flow of diabetic rats during a glucose challenge which could participate in the abnormal glucose-induced insulin secretion previously described in these two models. [Diabetologia (1994) 37: 677–680]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417691
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