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- Fetissov, SO, et al.
(författare)
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Autoantibodies against alpha -MSH, ACTH, and LHRH in anorexia and bulimia nervosa patients
- 2002
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 99:26, s. 17155-17160
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Tidskriftsartikel (refereegranskat)abstract
- The hypothalamic arcuate nucleus is involved in the control of energy intake and expenditure and may participate in the pathogenesis of eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). Two systems are of particular interest in this respect, synthesizing α-melanocyte-stimulating hormone (α-MSH) and synthesizing neuropeptide Y, respectively. We report here that 42 of 57 (74%) AN and/or BN patients studied had in their plasma Abs that bind to melanotropes and/or corticotropes in the rat pituitary. Among these sera, 8 were found to bind selectively to α-MSH-positive neurons and their hypothalamic and extrahypothalamic projections as revealed with immunostaining on rat brain sections. Adsorption of these sera with α-MSH peptide abolished this immunostaining. In the pituitary, the immunostaining was blocked by adsorption with α-MSH or adrenocorticotropic hormone. Additionally, 3 AN/BN sera bound to luteinizing hormone-releasing hormone (LHRH)-positive terminals in the rat median eminence, but only 2 of them were adsorbed with LHRH. In the control subjects, 2 of 13 sera (16%) displayed similar to AN/BN staining. These data provide evidence that a significant subpopulation of AN/BN patients have autoantibodies that bind to α-MSH or adrenocorticotropic hormone, a finding pointing also to involvement of the stress axis. It remains to be established whether these Abs interfere with normal signal transduction in the brain melanocortin circuitry/LHRH system and/or in other central and peripheral sites relevant to food intake regulation, to what extent such effects are related to and/or could be involved in the pathophysiology or clinical presentation of AN/BN, and to what extent increased stress is an important factor for production of these autoantibodies.
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- Grenback, E, et al.
(författare)
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Galanin in human plasma
- 2005
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Ingår i: Neuropeptides. - : Elsevier BV. - 0143-4179. ; 39:3, s. 337-340
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Tidskriftsartikel (refereegranskat)
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| 12. |
- Grenback, E, et al.
(författare)
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Galanin in pituitary adenomas
- 2004
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Ingår i: Regulatory peptides. - : Elsevier BV. - 0167-0115. ; 117:2, s. 127-139
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Tidskriftsartikel (refereegranskat)
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- Lindbom, U, et al.
(författare)
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Paradoxical GH response to TRH during status epilepticus in man
- 1999
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Ingår i: European journal of endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 140:4, s. 307-314
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Tidskriftsartikel (refereegranskat)abstract
- Information on GH in relation to epilepsy is sparse, and to our knowledge there is no information on GH levels during status epilepticus in man. We studied GH in serum in six patients during status epilepticus, and in a control group of six seizure-free patients with epilepsy, before and after injection of TRH. The baseline GH values before TRH administration were within the normal range in all patients. After injection of TRH all patients with status epilepticus showed a paradoxical peak-shaped increase of GH to at least twice their baseline levels within 45 min after the injection (median basal GH value 1.5 mU/l and median peak GH value 6. 5 mU/l, mean increase 330%). No uniform reaction to TRH was observed in the control group (median basal GH value 2.7 U/l and median of the highest value within 45 min 5.2mU/l). A paradoxical peak reaction of GH to TRH was significantly more frequent in the status epilepticus group compared with the control group (P=0.008, Fisher exact probability test). TRH is not considered a GH-releasing hormone in humans during normal conditions, but a paradoxical response of GH to TRH, similar to that observed during status epilepticus, has been reported in various other pathological conditions, such as acromegaly, liver cirrhosis, mental depression and hypothyroidism. Our results of GH release after TRH administration in patients with status epilepticus suggest an altered regulation of GH as a result of the long-standing epileptic activity.
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- Petersson, M, et al.
(författare)
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Long-term changes in gastrin, cholecystokinin and insulin in response to oxytocin treatment
- 1999
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Ingår i: Neuroendocrinology. - : S. Karger AG. - 0028-3835 .- 1423-0194. ; 69:3, s. 202-208
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Tidskriftsartikel (refereegranskat)abstract
- The present study was designed to investigate how repeated injections of oxytocin influence plasma levels of vagally controlled hormones such as gastrin, cholecystokinin (CCK), insulin and somatostatin, as well as of endogenous oxytocin and glucose. Since oxytocin may enhance the activity of centrally located α<sub>2</sub>-adrenoreceptors, a second aim of this study was to explore whether these receptors are involved in the effects. For this purpose, oxytocin (1.0 mg/kg) or NaCl was given subcutaneously (s.c.) once a day during 5 days to male rats. Rats were decapitated 1, 3 and 10 days after the last injection, blood was collected and hormone levels were radioimmunoassayed. The oxytocin treatment caused an elevation of plasma levels of oxytocin 1 day (p < 0.05) but not 3 and 10 days after treatment. Gastrin levels were decreased on day 1, 3 and 10 (ANOVA; p < 0.01). In addition, both insulin and CCK levels were decreased in response to the oxytocin treatment when measured 3 and 10 days after the last injection (ANOVA; insulin p < 0.01, CCK p < 0.05). When the α<sub>2</sub>-adrenoreceptor agonist clonidine (2.5 µg/kg intracerebroventricularly) was administered 3 days after the 5-day treatment period with oxytocin or saline, plasma levels of insulin and CCK increased significantly (p < 0.05) in the oxytocin-treated rats, when compared to saline-treated controls receiving clonidine only. No change in glucose or somatostatin levels was found in response to the oxytocin treatment. In conclusion, these results show that oxytocin induces long-lasting changes in plasma levels of gastrin, CCK and insulin, without affecting somatostatin or glucose levels. These effects may be mediated by changes in vagal nerve activity.
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- Stromberg, S, et al.
(författare)
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Pituitary autoantibodies in patients with hypopituitarism and their relatives
- 1998
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Ingår i: The Journal of endocrinology. - : Bioscientifica. - 0022-0795 .- 1479-6805. ; 157:3, s. 475-480
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Tidskriftsartikel (refereegranskat)abstract
- Autoantibodies to human pituitary cytosol proteins were determined by immunoblotting in sera from patients with hypopituitarism and their relatives. Reactivity to an M(r) 49,000 protein was significantly more frequent in patients (6/21 (28%) P < 0.05) as well as in relatives (10/35 (28%) P < 0.02) compared with controls (3/44 (6.8%)). Autoantibodies to this particular protein have previously been detected in sera from 70% of patients with biopsy-proven lymphocytic hypophysitis. Unlike patients with biopsy-proven lymphocytic hypophysitis, none of the patients in this study presented with a suspected pituitary adenoma or showed an enlarged sella turcica. Cisternal herniation was seen in 6/21 patients and this may very well represent the end stage of lymphocytic hypophysitis. Since organ specific autoantibodies are frequent in patients with autoimmune endocrine disease as well as in their unaffected relatives, autoantibodies to this M(r) 49,000 pituitary cytosolic protein may represent markers for an immunological process affecting the pituitary gland.
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