| 21. |
- Karefylakis, Christos, 1982-, et al.
(författare)
-
Vitamin D Status 10 Years After Primary Gastric Bypass : Gravely High Prevalence of Hypovitaminosis D and Raised PTH Levels
- 2014
-
Ingår i: Obesity Surgery. - : Springer Science and Business Media LLC. - 0960-8923 .- 1708-0428. ; 24:3, s. 343-348
-
Tidskriftsartikel (refereegranskat)abstract
- The primary aim of this study was to evaluate the prevalence of vitamin D deficiency and secondary hyperparathyroidism after Roux-en-Y gastric bypass. Secondly, we have tried to assess predictors for vitamin D deficiency. Five hundred thirty-seven patients who underwent primary Roux-en-Y gastric bypass surgery between 1993 and 2003 at the A-rebro University Hospital and Uppsala University Hospital were eligible for the study. Patients were asked to provide a blood sample between November 2009 and June 2010 and to complete a questionnaire about their postoperative health status. Serum values of 25-OH vitamin D, parathyroid hormone (PTH), alkaline phosphatase (ALP) and calcium were determined. Follow-up was completed in 293 patients, of which 83 % were female, with an age of 49 +/- 9.9 years after a median time of 11 +/- 2.8 years. Vitamin D, PTH and albumin-corrected calcium values were 42 +/- 20.4 nmol/L, 89.1 +/- 52.7 ng/L and 2.3 +/- 0.1 mmol/L, respectively. Of all patients, 65 % were vitamin D deficient, i.e. 25-OH vitamin D < 50 nmol/L, and 69 % had PTH above the upper normal reference range, i.e. > 73 ng/L. Vitamin D was inversely correlated with PTH levels (p < 0.001) and positively correlated with calcium (p = 0.016). Vitamin D did not correlate with ALP. The only factor found to predict vitamin D deficiency was high preoperative body mass index (BMI) (p = 0.008), whereas gender, age, time after surgery and BMI at follow-up did not. Vitamin D deficiency and secondary hyperparathyroidism after Roux-en-Y gastric bypass (RYGB) were confirmed in our study because 65 % of patients had vitamin D deficiency, and 69 % had increased PTH levels more than 10 years after surgery. These data are alarming and highlight the need for improved long-term follow-up. Vitamin D deficiency does not seem to progress with time after surgery, possibly due to weight loss. Only preoperative BMI, cutoff point 43 kg/m(2), was a predictor of vitamin D deficiency at follow-up. Improved long-term follow-up of patients that undergo RYGB is needed.
|
|
| 22. |
- Mattsson, Cecilia, et al.
(författare)
-
Gender-specific links between hepatic 11beta reduction of cortisone and adipokines
- 2007
-
Ingår i: Obesity. - : Wiley. - 1930-7381 .- 1930-739X. ; 15:4, s. 887-894
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Reduction of cortisone to cortisol is mediated by 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1), a putative key enzyme in obesity-related complications. Experimental studies suggest that adipokines, notably leptin and tumor necrosis factor-alpha (TNF-alpha), are of importance for 11betaHSD1 activity. We hypothesized that the regulation of hepatic preceptor glucocorticoid metabolism is gender-specific and associated with circulating levels of leptin and TNF-alpha receptors and/or sex hormones. RESEARCH METHODS AND PROCEDURES: A total of 34 males and 38 women (14 premenopausal and 22 postmenopausal) underwent physical examination and fasting blood sampling. Insulin sensitivity was tested by euglycemic hyperinsulinemic clamps, and hepatic 11betaHSD1 enzyme activity was estimated by the conversion of orally-ingested cortisone to cortisol. RESULTS: Hepatic 11betaHSD1 activity was negatively associated with leptin and soluble TNF (sTNF) r1 and sTNFr2 in males. These correlations remained significant after adjustment for age and insulin sensitivity, and for sTNF-alpha receptors also after adjustment of BMI and waist circumference. In contrast, 11beta reduction of cortisone was positively associated to leptin in females after adjustment for BMI and waist circumference. DISCUSSION: Hepatic 11beta reduction shows different links to circulating adipocyte-derived hormones in males and females. This emphasizes the need for further studies on tissue-specific regulation of 11betaHSD1 in both genders.
|
|
| 23. |
|
|
| 24. |
- Rask, Eva, 1958-, et al.
(författare)
-
Adrenocorticotropin-independent Cushing's syndrome in pregnancy related to overexpression of adrenal luteinizing hormone/human chorionic gonadotropin receptors
- 2009
-
Ingår i: Journal of Endocrinological Investigation. - : Editrice kurtis. - 0391-4097 .- 1720-8386. ; 32:4, s. 313-316
-
Tidskriftsartikel (refereegranskat)abstract
- Cushing's syndrome during pregnancy is rare, and rather than being of pituitary origin most patients exhibit ACTH-independent adrenal hypercortisolism. In some cases the syndrome has spontaneously resolved post partum, suggesting the presence of a pregnancy-associated stimulatory factor(s). We describe a case with aberrant adrenal LH/hCG receptors in a large adrenal tumor as a possible explanation for cortisol hypersecretion and tumor growth in Cushing s syndrome during pregnancy. A 27-yr-old woman presented with hypertension and diabetes mellitus in early pregnancy. Investigations revealed hypercortisolemia, suppressed ACTH-levels, and a 6.4- cm right adrenal tumor. The tumor was successfully removed by laparoscopy at 26th week of pregnancy. Hypercortisolism and hypertension resolved post-operatively. The tumor displayed higher LH/hCG receptor mRNA and protein positivity than adjacent normal adrenal tissue as examined by in situ hybridization and immunocytochemistry. High physiological levels of hCG, in conjunction with aberrant adrenal LH/hCG receptor overexpression, may have contributed to the development of Cushing's syndrome in pregnancy.
|
|
| 25. |
- Rask, Eva, 1958-, et al.
(författare)
-
Cortisol metabolism after weight loss : associations with 11 beta-HSD type 1 and markers of obesity in women
- 2013
-
Ingår i: Clinical Endocrinology. - : Wiley. - 0300-0664 .- 1365-2265. ; 78:5, s. 700-705
-
Tidskriftsartikel (refereegranskat)abstract
- 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.
|
|
| 26. |
|
|
| 27. |
|
|
| 28. |
- Rask, Eva, 1958-, et al.
(författare)
-
Impaired incretin response after a mixed meal is associated with insulin resistance in nondiabetic men
- 2001
-
Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 24:9, s. 1640-1645
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:To investigate whether features of the insulin resistance syndrome are associated with altered incretin responses to food intake.RESEARCH DESIGN AND METHODS:From a population-based study, 35 men were recruited, representing a wide spectrum of insulin sensitivity and body weight. Each subject underwent a hyperinsulinemic-euglycemic clamp to determine insulin sensitivity. A mixed meal was given, and plasma levels of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), as well as insulin, glucagon, and glucose were measured.RESULTS:Insulin resistance was associated with impaired GIP and GLP-1 responses to a mixed meal. The total area under the curve (AUC) of the GIP response after the mixed meal was associated with insulin sensitivity (r = 0.54, P < 0.01). There was a significant difference between the highest and the lowest tertile of insulin sensitivity (P < 0.05). GLP-1 levels 15 min after food intake were significantly lower in the most insulin-resistant tertile compared with the most insulin-sensitive tertile. During the first hour, the AUC of GLP-1 correlated significantly with insulin sensitivity (r = 0.47, P < 0.01). Multiple linear regression analysis showed that insulin resistance, but not obesity, was an independent predictor of these decreased incretin responses.CONCLUSIONS:In insulin resistance, the GIP and GLP-1 responses to a mixed meal are impaired and are related to the degree of insulin resistance. Decreased incretin responsiveness may be of importance for the development of impaired glucose tolerance.
|
|
| 29. |
|
|
| 30. |
- Rask, Eva, 1958-, et al.
(författare)
-
[Report of a case. Inhalation steroids caused adrenal cortex suppression]
- 1997
-
Ingår i: Läkartidningen. - : Läkartidningen Förlag AB. - 0023-7205 .- 1652-7518. ; 94:40, s. 3529-30, 3533
-
Tidskriftsartikel (refereegranskat)abstract
- In one of two cases of systemic effects of high-dose inhaled corticosteroid treatment with fluticasone propionate, adrenal suppression was demonstrated in a young man, and in the other retarded growth and severe general effects were observed in connection with infection in a child. These cases illustrate the risk of systemic effects of inhaled corticosteroids, and the importance of using the lowest possible maintenance dose.
|
|
