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  • 1.
    Alvehus, M.
    et al.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Simonyte, K.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Andersson, T.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Söderström, I.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Burén, J.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Rask, Eva
    Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Mattsson, C.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Olsson, T.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå University, Umeå, Sweden.
    Adipose tissue IL-8 is increased in normal weight women after menopause and reduced after gastric bypass surgery in obese women2012In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 77, no 5, p. 684-690Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE:

    The menopausal transition is characterized by increased body fat accumulation, including redistribution from peripheral to central fat depots. This distribution is associated with an increased risk of type 2 diabetes and cardiovascular disease that are linked to low-grade inflammation. We determined whether postmenopausal women have higher levels of inflammatory markers, compared with premenopausal women. We also wanted to determine whether these markers are reduced by stable weight loss in obese women.

    DESIGN AND METHODS:

    Anthropometric data, blood samples and subcutaneous adipose tissue biopsies were collected from normal weight premenopausal and postmenopausal women and obese women before and 2 years after gastric bypass (GBP) surgery. Serum protein levels and adipose tissue gene expression of inflammatory markers were investigated.

    RESULTS:

    IL-8 expression in adipose tissue and circulating levels were higher in postmenopausal vs premenopausal women. IL-8 expression was associated with waist circumference, independent of menopausal status. IL-6 expression and serum levels of monocyte chemoattractant protein (MCP)-1 were higher in postmenopausal vs premenopausal women. Two years after GBP surgery, adipose expression of IL-8, tumour necrosis factor-α and MCP-1 decreased significantly. Serum insulin levels were associated with inflammation-related gene expression before GBP surgery, but these associations disappeared after surgery.

    CONCLUSION:

    Postmenopausal women have an increased inflammatory response in the subcutaneous fat and circulation. Inflammatory markers in adipose tissue decreased significantly after surgery-induced weight loss. This effect may be beneficial for metabolic control and reduced cardiovascular risk after weight loss.

  • 2.
    Jendle, Johan
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Endocrine and Diabetes Center, Karlstad Hospital, Karlstad, Sweden.
    Christensen, Jane H.
    Department of Biomedicine, Aarhus University, Aarhus, Denmark; Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark .
    Kvistgaard, Helene
    Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
    Gregersen, Niels
    Research Unit for Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark.
    Rittig, Søren
    Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
    Late-onset familial neurohypophyseal diabetes insipidus due to a novel mutation in the AVP gene2012In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 77, no 4, p. 586-592Article in journal (Refereed)
    Abstract [en]

    Objective: Familial neurohypophyseal diabetes insipidus (FNDI) is mainly an autosomal dominant inherited disorder presenting with severe polydipsia and polyuria in early childhood. In this study, we aimed to determine the molecular genetics and clinical characteristics of a large Swedish-Norwegian family presenting with very late-onset autosomal dominant FNDI.

    Patients: Six probands with a history of developing polyuria and polydipsia during adolescence were studied.

    Measurements: Information on family demography was collected by personal interview with family members. The genetic cause of FNDI was identified by DNA sequencing analysis of the coding regions of the AVP gene. The clinical characteristics were determined by the measurement of basal urine production and osmolality as well as by measurements of concurrent levels of plasma AVP, plasma osmolality, and urine osmolality during fluid deprivation and bolus injection of DDAVP. The integrity of the neurohypophysis was evaluated by magnetic resonance imaging.

    Results: The mean age of encountering the first clinical symptoms in the family was 14·8 years (range 3-30 years) (n = 17). All six affected subjects investigated were heterozygous for a novel mutation in the AVP gene (g.1848C>T) predicting a p.Pro84Leu substitution in the AVP precursor protein. We found partial deficiency in evoked AVP secretion during fluid deprivation in one subject and complete deficiency in another. The pituitary bright spot was absent in all six affected subjects studied.

    Conclusion: A novel mutation in the AVP gene predicted to cause a neurophysin II dimerization defect is causing surprisingly late onset of FNDI in a large, six generation, Swedish-Norwegian family. The mutation is associated with both complete and partial deficiency in evoked AVP secretion during fluid deprivation in patients who have suffered from FNDI for decades.

  • 3.
    Nygren, J
    et al.
    Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Sammann, Michael
    Department of Plastic Surgery, Karolinska Hospital, Stockholm, Sweden.
    Malm, Mats
    Department of Plastic Surgery, Karolinska Hospital, Stockholm, Sweden.
    Efendic, Suad
    Department of Endocrinology, Karolinska Hospital, Stockholm, Sweden.
    Hall, Kerstin
    Department of Endocrinology, Karolinska Hospital, Stockholm, Sweden.
    Brismar, Kerstin
    Department of Endocrinology, Karolinska Hospital, Stockholm, Sweden.
    Ljungqvist, Olle
    Örebro University, School of Medical Sciences. Department of Surgery, Karolinska Hospital, Stockholm, Sweden.
    Disturbed anabolic hormonal patterns in burned patients: the relation to glucagon1995In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 43, no 4, p. 491-500Article in journal (Refereed)
    Abstract [en]

    Objective. Complex changes in the anabolic regulators of metabolism occur after major injury. We have studied the time course for IGF-I and IGFBP-1 after burn injury and their relations to circulating levels of other anabolic and catabolic hormones. The hormonal patterns during the onset of sepsis were also investigated. Patients. Eight patients (age 36 (6) years, mean (SEM)) with major burn injury (burn area 42 (6)%) were studied. The first 2 days since the burn were used for rehydration therapy (rehydration period), after which a complete total parenteral nutrition (TPN) period was initiated. Seven of the eight patients developed sepsis, confirmed with positive blood cultures, during the study period. Six of the eight survived. Measurements. The hormonal changes determined inthe morning during the first 7 days after the burn and from day 22 to 24 were investigated. The superimposed effects of sepsis were studied by normalizing all data to the day of positive blood cultures and clinical onset of sepsis. Results. On admission, plasma levels of glucagon, IGFBP-1 and GH were elevated while levels of IGF-I were low. During the first week after the burn, morning levels of glucagon and insulin increased while levels of GH and IGF-I decreased. GH levels were still elevated compared to healthy subjects. Despite the increase in insulin levels, IGFBP-1 remained elevated. Three weeks after the burn injury, IGF-I levels were increased but still markedly below normal, while IGFBP-1 levels remained unchanged. Persistent elevations of insulin levels were combined with reductions in glucagon levels. Admission levels of IGFBP-1 correlated to nitrogen loss (negative nitrogen balance) during the first 24 hours after the burn (r = 0.84, P < 0.05). A correlation between negative nitrogen balance and glucagon levels was found during the early catabolic period in the rehydration period (i.e. days 2-3, r = 0.84, P < 0.01). The relative change in IGFBP-1 levels in the rehydration period correlated to changes in glucagon levels (days 2-3 vs admission, r = 0.65, P < 0.05). The insulin/glucagon molar ratio correlated to the IGF-I/IGFBP-1 ratio during both the rehydration period (days 2-3, r = 0.77, P < 0.05) and the third week after the burn (r = 0.77, P < 0.05). During the most catabolic phase in the first week after the burn (TPN period) there was an inverse relation between IGF-I and IGFBP-1 levels (r = -0.83, P < 0.05). During the less catabolic third week after the burn, an inverse correlation was found between IGF-I and glucagon (r = -0.83, P < 0.05). Sepsis, superimposed upon the burn trauma, was associated with transient elevations in IGFBP-1 and reductions in insulin despite elevated levels of glucose and a further 50% increase in nitrogen losses. Conclusions. The present findings show that marked changes in important anabolic regulating factors occur after major burn injury. Uncoupling of the GH-IGF-I axis, and the attenuation of the inhibitory effects of insulin on IGFBP-1, both contribute to the reduction in IGF-I levels and bioavailability, factors which may play an important role in post injury metabolism. Furthermore, these data suggest that of the catabolic hormones (catecholamines, cortisol and glucagon), primarily glucagon seem to be involved in the modulation of IGF-I and IGFBP-1 levels following burn injury.

  • 4.
    Rask, Eva
    et al.
    Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Simonyte, K.
    Umeå University, Umeå, Sweden.
    Lonn, L.
    Rigshospitalet, Copenhagen, Denmark .
    Axelson, M.
    Karolinska University Hospital, Stockholm, Sweden.
    Cortisol metabolism after weight loss: associations with 11 beta-HSD type 1 and markers of obesity in women2013In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 78, no 5, p. 700-705Article in journal (Refereed)
    Abstract [en]

    Objective Increased glucocorticoid metabolite excretion and enhanced expression and activity of 11-hydroxysteroid dehydrogenase type 1 in adipose tissue are closely correlated with obesity and its detrimental consequences. Weight loss ameliorates the latter. The aim of this study was to explore whether increased glucocorticoid exposure in obesity is improved with substantial weight loss and thus is a consequence rather than a cause of obesity.

    Design and patients A prospective cohort study in 31 women.

    Measurements 11-HSD type 1 expression and activity, urinary glucocorticoid metabolite excretion, body composition including regional adipose tissue depots and insulin resistance by HOMA-IR before and 2years after gastric bypass surgery.

    Results After weight loss, excretion of cortisol and cortisone metabolites decreased. Both cortisol and cortisone metabolite excretion correlated with central obesity, where the intraabdominal fat depot showed the strongest association. Cortisol metabolites correlated with 11-HSD type 1 activity in abdominal subcutaneous adipose tissue. The ratio of cortisol to cortisone metabolites [(5-tetrahydrocortisol (5THF)+tetrahydrocortisol (THF)+-cortol)/(tetrahydrocortisone (THE)+-cortolone)] and the ratio of 5-THF/THF both decreased after stable weight loss, reflecting a downregulation of the net activities of 11-HSD type 1 and 5-reductase.

    Conclusion Long-term weight loss in women is not only followed by reduced glucocorticoid production, but also favourably decreases the global and tissue-specific activity of the cortisol-activating enzyme 11 -HSD type 1, possibly contributing to the health benefits of bariatric surgery.

  • 5.
    Wake, Deborah J.
    et al.
    Endocrinology Unit, Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
    Strand, Magnus
    Department of Medicine, Umeå University Hospital, Umeå, Sweden.
    Rask, Eva
    Department of Medicine, Umeå University Hospital, Umeå, Sweden.
    Westerbacka, Jukka
    Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland.
    Livingstone, Dawn E. W.
    Endocrinology Unit, Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
    Soderberg, Stefan
    Department of Medicine, Umeå University Hospital, Umeå, Sweden.
    Andrew, Ruth
    Endocrinology Unit, Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
    Yki-Jarvinen, Hannele
    Department of Medicine, Division of Diabetes, University of Helsinki, Helsinki, Finland.
    Olsson, Tommy
    Department of Medicine, Umeå University Hospital, Umeå, Sweden.
    Walker, Brian R.
    Endocrinology Unit, Queen's Medical Research Institute, University of Edinburgh, United Kingdom; dEndocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, United Kingdom.
    Intra-adipose sex steroid metabolism and body fat distribution in idiopathic human obesity2007In: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 66, no 3, p. 440-6Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Causes of visceral fat accumulation include glucocorticoid excess or decreased oestrogen/androgen ratio either in plasma or within adipose tissue. In obese subjects, the intra-adipose cortisol-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is increased, but information on sex steroid signalling is sparse. We aimed to test associations between body fat or fat distribution and mRNA transcript levels for androgen and oestrogen receptors and for enzymes metabolizing sex steroids in adipose tissue.

    DESIGN: A cross-sectional study.

    PATIENTS: Forty-five healthy men and women with body mass index (BMI) 21-36 kg/m(2).

    MEASUREMENTS: In subcutaneous adipose biopsies we measured mRNAs for enzymes metabolizing local oestrogens (aromatase) and androgens [5alpha-reductase type 1; AKR1C2 (3alpha-HSD3); AKR1C3 (17beta-HSD5, 3alpha-HSD2)] and for sex steroid receptors [oestrogen receptor (ER)-alpha and androgen receptor (AR)]. We related these to body fat mass and distribution.

    RESULTS: Generalized obesity (BMI) was associated with increased aromatase mRNA (r = 0.35, P < 0.05). Central obesity (waist : hip ratio) was associated with mRNA for AKR1C2 (r = 0.28, P < 0.05) and AKR1C3 (r = 0.38, P < 0.01) but not aromatase (r = 0.06). 5alpha-Reductase type 1, ER and AR mRNA levels did not predict fat amount or its distribution.

    CONCLUSION: These data on transcript levels suggest that, in idiopathic obesity, increased intra-adipose oestrogen generation by aromatase predicts peripheral fat distribution, while androgen metabolism by AKR1C isoforms predicts central fat distribution, supporting the hypothesis that intra-adipose sex steroid metabolism is a determinant of gynoid vs. android patterns of body fat.

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