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| 2. |
- Florén, Claes-Henrik, et al.
(författare)
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Bone mineral density in patients with Crohn's disease during long-term treatment with azathioprine
- 1998
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Ingår i: Journal of Internal Medicine. - 1365-2796. ; 243:2, s. 123-126
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To ascertain whether patients with Crohn's disease treated with azathioprine maintained bone mineral mass better than patients treated with steroids alone. DESIGN: Retrospective study. SETTING: University Hospital of Malmo, Sweden. SUBJECTS: A total of 59 patients with ileocolonic, ileocaecal or colonic Crohn's disease. METHODS: Bone mass was assessed by dual photon X-ray absorptiometry at the level of L2-L4. RESULTS: Patients treated with a high lifetime dose of steroids (> 5 g prednisolone) had significantly (P = 0.011) lower Z-score of L2-L4 (-0.87 +/- 1.11; 11 SD) than steroid-treated patients, who had received a low dose of prednisolone (< 5 g) (0.08 +/- 1.16 SD). Azathioprine did not negatively influence the steroid effect on bone mineral density. CONCLUSIONS: Azathioprine does not seem to affect bone mineral density by itself. However, by being steroid-saving, it seems to conserve bone mineral mass in patients with Crohn's disease.
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| 4. |
- Larsson, Hillevi, et al.
(författare)
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Evidence for leptin regulation of food intake in humans
- 1998
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 83:12, s. 4382-4385
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Tidskriftsartikel (refereegranskat)abstract
- The adipocyte hormone leptin regulates body weight in mice by decreasing food intake and increasing energy expenditure. Whether leptin is of physiological importance for these processes in humans is, however, not clear. We therefore studied the relation between leptin and habitual food intake in 64 healthy postmenopausal women. Dietary habits were assessed with a modified diet history method. Body fat content was measured using bioelectrical impedance. In the 64 women, aged 58.6 ± 0.4 yr (mean ± SD), serum leptin was 19.3 ± 12.7 ng/mL, body mass index was 25.0 ± 3.5 kg/m2, body fat content was 31.6 ± 4.3%, fasting glucose was 4.6 ± 0.5 mmol/L, and fasting insulin was 56 ± 21 pmol/L. Leptin levels were negatively correlated to total energy intake (r = -0.34; P = 0.006), carbohydrate intake (r = - 0.36; P = 0.004), and total (r = -0.27; P = 0.034) as well as saturated fat intake (r = -0.31; P = 0.014). Leptin was correlated to the absolute, but not to the percent, intake of these nutrients. When normalized for body fat content, the correlations remained significant. Our results suggest that plasma leptin is involved in the physiological regulation of food intake in humans, and that leptin is related to the quantity rather than the quality of habitual food intake.
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| 5. |
- Mulder, Hindrik, et al.
(författare)
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Hormone-sensitive lipase, the rate-limiting enzyme in triglyceride hydrolysis, is expressed and active in beta-cells
- 1999
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Ingår i: Diabetes. - 1939-327X. ; 48:1, s. 228-232
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Tidskriftsartikel (refereegranskat)abstract
- Triglycerides in the beta-cell may be important for stimulus-secretion coupling, through provision of a lipid-derived signal, and for pathogenetic events in NIDDM, where lipids may adversely affect beta-cell function. In adipose tissues, hormone-sensitive lipase (HSL) is rate-limiting in triglyceride hydrolysis. Here, we investigated whether this enzyme is also expressed and active in beta-cells. Northern blot analysis and reverse transcription-polymerase chain reaction demonstrated that HSL is expressed in rat islets and in the clonal beta-cell lines INS-1, RINm5F, and HIT-T15. Western blot analysis identified HSL in mouse and rat islets and the clonal beta-cells. In mouse and rat, immunocytochemistry showed a predominant occurrence of HSL in beta-cells, with a presumed cytoplasmic localization. Lipase activity in homogenates of the rodent islets and clonal beta-cells constituted 2.1 +/- 0.6% of that in adipocytes; this activity was immunoinhibited by use of antibodies to HSL. The established HSL expression and activity in beta-cells offer a mechanism whereby lipids are mobilized from intracellular stores. Because HSL in adipocytes is activated by cAMP-dependent protein kinase (PKA), PKA-regulated triglyceride hydrolysis in beta-cells may participate in the regulation of insulin secretion, possibly by providing a lipid-derived signal, e.g., long-chain acyl-CoA and diacylglycerol.
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| 6. |
- Stenson, Lena, et al.
(författare)
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Protein kinase B is expressed in pancreatic beta cells and activated upon stimulation with insulin-like growth factor I
- 1998
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Ingår i: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 250:1, s. 181-186
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Tidskriftsartikel (refereegranskat)abstract
- Protein kinase B (PKB) is involved in signaling to a multitude of important cellular events and is activated by insulin and growth factors, including insulin-like growth factor I (IGF-I). We show here expression of PKB in pancreatic islets and in the beta cell lines HIT-T15, INS-1, and RINm5F. Expression of PKB mRNA and the presence of PKB isoforms (alpha, beta, and gamma) were assessed by Northern blot analysis and RT-PCR, respectively. Antibodies recognizing different parts of PKB isoforms were employed to demonstrate PKB protein expression by immunoblot analysis. By use of immunohistochemistry in rat and mouse pancreatic tissue sections, PKB was localized to predominantly beta cells. Regulation of PKB was examined in INS-1 and RINm5F cells; upon stimulation with IGF-I (5-10 min), PKB was phosphorylated and activated (approximately 3-fold) by a wortmannin-sensitive mechanism, indicating involvement of phosphatidylinositol-3 kinase. The possible participation of PKB in signal transduction pathways modulating cAMP-dependent insulin secretion and in proliferation of beta cells is discussed.
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