| 51. |
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| 52. |
- Karlsson, C, et al.
(författare)
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Human adipose tissue expresses angiotensinogen and enzymes required for its conversion to angiotensin II.
- 1998
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Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 83:11, s. 3925-9
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Tidskriftsartikel (refereegranskat)abstract
- Angiotensin II regulates blood pressure and may affect adipogenesis and adipocyte metabolism. Angiotensin II is produced by cleavage of angiotensinogen by renin and angiotensin-converting enzyme in the circulation. In addition, angiotensin II may be produced in various tissues by enzymes of the renin-angiotensin system (RAS) or the nonrenin-angiotensin system (NRAS). We have analyzed the expression of angiotensinogen and enzymes required for its conversion to angiotensin II in human adipose tissue. Northern blot demonstrated angiotensinogen expression in adipose tissue from nine obese subjects. Western blot revealed a distinct band of expected size of the angiotensinogen protein (61 kDa) in isolated adipocytes. RT-PCR, followed by Southern blot, demonstrated renin expression in human adipose tissue. Angiotensin-converting enzyme messenger RNA was detected by RT-PCR, and the identity of the PCR products was verified by restriction enzyme cleavage. Transcripts for cathepsin D and cathepsin G, components of the NRAS, were detected by RT-PCR, verified by restriction enzyme cleavage. We conclude that human adipose tissue expresses angiotensinogen and enzymes of RAS and NRAS. This opens the possibility that angiotensinogen-derived peptides, produced in adipose tissue itself, may affect adipogenesis and play a role in the pathogenesis of obesity.
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| 53. |
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| 54. |
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| 55. |
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| 56. |
- Kriström, Berit, et al.
(författare)
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Growth response to growth hormone (GH) treatment relates to serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 in short children with various GH secretion capacities. Swedish Study Group for Growth Hormone Treatment.
- 1997
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - 0021-972X .- 1945-7197. ; 82:9, s. 2889-98
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the study was to evaluate the relationship between the 1-yr (n = 193) and 2-yr (n = 128) growth response and the individual serum concentrations of insulin-like growth factor I (IGF-I) and IGF-binding protein 3 (IGFBP-3) before and during GH treatment. Our study group of prepubertal short children had from very low to high GH secretory capacity, estimated during an arginine-insulin tolerance test, and the ages ranged from 3-15 yr at the start of treatment. Their serum levels of IGF-I and IGFBP-3 were low before treatment compared to those in an age-related reference group of prepubertal children and increased significantly from the start to 1 month of GH treatment. The mean increase in height SD score was 0.80 SD score after 1 yr of GH treatment and 1.26 SD score after 2 yr, with a wide range. In univariate analyses the highest correlation coefficients to the 2-yr growth response were found to be vs. the following variables from the start of treatment: IGF-I SD score (r = -0.49), log maximum GH concentration (log GHmax) during the arginine-insulin tolerance test (r = -0.47), difference between the height SD score of the individual child and the midparental height SD score (diffSD score; r = -0.45), IGFBP-3 SD score (r = -0.39), age (r = -0.30), short term change in IGFBP-3 SD score (r = 0.37), and IGF-I SD score (r = 0.34). In multivariate stepwise regression analysis, 41% of the variation in the 2-yr growth response could be explained by IGF-I SD score or log GHmax together with age at the start of treatment, weight SD score at 1 yr of age, and diffSD score. When both IGF-I SD score and GHmax were included and when the short term changes in IGF-I SD score were added, 46% and 58% of the variation, respectively, could be explained. The regression algorithms using different combinations of variables and their corresponding prediction intervals are also presented.
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| 57. |
- Kriström, Berit, et al.
(författare)
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Short-term changes in serum leptin levels provide a strong metabolic marker for the growth response to growth hormone treatment in children. Swedish Study Group for Growth Hormone Treatment.
- 1998
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - 0021-972X .- 1945-7197. ; 83:8, s. 2735-41
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Tidskriftsartikel (refereegranskat)abstract
- The growth response to GH treatment varies between children. Besides regulating longitudinal growth, GH exerts important metabolic effects, including lipolysis. In this study we examined whether GH-induced changes in serum levels of the adipose tissue-derived hormone leptin can be used as a marker for the long term growth response to GH treatment in short prepubertal children. The study group consisted of 150 children (21 girls and 129 boys), who were 3-15 yr of age at the start of GH treatment and had a maximum GH secretory capacity ranging from very low to high. They were treated with GH (0.1 IU/kg x day) and followed for at least 1 yr. The first year mean increase in height SD score was 0.79 (SD, 0.34), with a broad range (0.08-2.27). Serum leptin concentrations were significantly reduced after 1, 3, and 12 months of GH treatment compared with levels at the start of treatment. The growth response correlated with the serum leptin concentration at the start of treatment (r = 0.49; P < 0.0001) and with the change in serum leptin concentration after both 1 month (r = -0.41; P < 0.01) and 3 months (r = -0.60; P < 0.0001) of treatment. When multiple stepwise regression analysis was applied to the auxological and biochemical variables that correlated (P < 0.10) with the first year growth response to GH treatment, the 3-month change in serum leptin concentration was the single most important variable for explaining the variance in individual growth responses. We conclude that leptin levels at the start of GH treatment as well as short term changes in leptin levels in response to GH treatment are valuable markers of the long term growth response.
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| 58. |
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| 59. |
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| 60. |
- 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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