| 1. |
- Al-Qahtani, SM, et al.
(författare)
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17β-Estradiol suppresses visceral adipogenesis and activates brown adipose tissue-specific gene expression
- 2017
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891 .- 1868-1883. ; 29:1, s. 13-26
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Tidskriftsartikel (refereegranskat)abstract
- Both functional ovaries and estrogen replacement therapy (ERT) reduce the risk of type 2 diabetes (T2D). Understanding the mechanisms underlying the antidiabetic effects of 17β-estradiol (E2) may permit the development of a molecular targeting strategy for the treatment of metabolic disease. This study examines how the promotion of insulin sensitivity and weight loss by E2 treatment in high-fat-diet (HFD)-fed mice involve several anti-adipogenic processes in the visceral adipose tissue. Magnetic resonance imaging (MRI) revealed specific reductions in visceral adipose tissue volume in HFD+E2 mice, compared with HFD mice. This loss of adiposity was associated with diminished visceral adipocyte size and reductions in expression of lipogenic genes, adipokines and of the nuclear receptor
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| 2. |
- Fahlén, M, et al.
(författare)
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Megestrol acetate may stimulate the production of insulin-like growth factor 1 in breast tissues of women with breast cancer
- 2013
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891 .- 1868-1883. ; 13:3, s. 51-4
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Tidskriftsartikel (refereegranskat)abstract
- In women with breast cancer who were treated with either continuous tamoxifen alone or sequential tamoxifen followed by megestrol acetate (MA), we demonstrated significant positive associations between the breast tumor estrogen receptor (ER) and an increase in serum sex hormone-binding globulin (SHBG) during tamoxifen treatment. We interpreted this as “ER uniformity” in different tissues, e.g., breast, liver. No other associations with ER were found. In the same study, the breast tumor progesterone receptor (PR) was determined. Our aim was to see if there were any associations between PR and endocrine changes during MA treatment.The breast tumor PR before treatment and serum insulin-like growth factor I (∂IGF-1), steroids, steroid-binding proteins, and insulin before and during treatment were measured in 17 postmenopausal women with breast cancer who were treated sequentially with tamoxifen 40 mg/day followed by MA 160 mg/day in alternating 3-month periods.During MA treatment periods, the levels of IGF-1 and insulin increased significantly, whereas the levels of androgens, SHBG, corticosteroid-binding globulin, and cortisol decreased significantly. Significant positive correlations were found between the PR content and increments in ∂IGF-1 but not between PR and any other endocrine change.PR expression in human liver is very weak, but malignant and normal breast tissues secrete considerable amounts of growth hormone and IGF-1 in vitro and in vivo. This activity is stimulated by progestogens. The association between PR and ∂IGF-1 may therefore reflect a direct PR-mediated action of MA on malignant and normal human breast tissues in vivo.
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| 3. |
- Gao, H, et al.
(författare)
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Implications of estrogen receptor alpha and estrogen receptor beta for adipose tissue functions and cardiometabolic complications
- 2013
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891 .- 1868-1883. ; 15:3, s. 81-90
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Tidskriftsartikel (refereegranskat)abstract
- There is growing evidence that estrogen signaling regulates energy metabolism and exerts important functions in maintaining adipose tissue metabolism, including controlling the distribution of body fat. Changes in the physiological functions of adipose tissue, particularly the white adipose tissue, have been strongly connected to obesity and the development of related cardiometabolic complications. In this review, we will focus on discussing the role of estrogen signaling in regulating adipocyte differentiation, metabolism and its endocrine function with a focus on the possible underlying molecular mechanisms mediated by estrogen receptor α and estrogen receptor β.
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| 4. |
- Green, Charlotte J., et al.
(författare)
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Studying non-alcoholic fatty liver disease : the ins and outs of in vivo, ex vivo and in vitro human models
- 2020
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Ingår i: Hormone Molecular Biology and Clinical Investigation. - : Walter de Gruyter GmbH. - 1868-1883 .- 1868-1891. ; 41:1
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Forskningsöversikt (refereegranskat)abstract
- The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing. Determining the pathogenesis and pathophysiology of human NAFLD will allow for evidence-based prevention strategies, and more targeted mechanistic investigations. Various in vivo, ex situ and in vitro models may be utilised to study NAFLD; but all come with their own specific caveats. Here, we review the human-based models and discuss their advantages and limitations in regards to studying the development and progression of NAFLD. Overall, in vivo whole-body human studies are advantageous in that they allow for investigation within the physiological setting, however, limited accessibility to the liver makes direct investigations challenging. Non-invasive imaging techniques are able to somewhat overcome this challenge, whilst the use of stable-isotope tracers enables mechanistic insight to be obtained. Recent technological advances (i.e. normothermic machine perfusion) have opened new opportunities to investigate whole-organ metabolism, thus ex situ livers can be investigated directly. Therefore, investigations that cannot be performed in vivo in humans have the potential to be undertaken. In vitro models offer the ability to perform investigations at a cellular level, aiding in elucidating the molecular mechanisms of NAFLD. However, a number of current models do not closely resemble the human condition and work is ongoing to optimise culturing parameters in order to recapitulate this. In summary, no single model currently provides insight into the development, pathophysiology and progression across the NAFLD spectrum, each experimental model has limitations, which need to be taken into consideration to ensure appropriate conclusions and extrapolation of findings are made.
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| 5. |
- Honek, J, et al.
(författare)
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Brown adipose tissue, thermogenesis, angiogenesis: pathophysiological aspects
- 2014
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891 .- 1868-1883. ; 19:1, s. 5-11
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Tidskriftsartikel (refereegranskat)abstract
- The number of obese and overweight individuals is globally rising, and obesity-associated disorders such as type 2 diabetes, cardiovascular disease and certain types of cancer are among the most common causes of death. While white adipose tissue is the key player in the storage of energy, active brown adipose tissue expends energy due to its thermogenic capacity. Expanding and activating brown adipose tissue using pharmacological approaches therefore might offer an attractive possibility for therapeutic intervention to counteract obesity and its consequences for metabolic health.
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| 6. |
- Mastinu, A, et al.
(författare)
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Cannabinoids in health and disease: pharmacological potential in metabolic syndrome and neuroinflammation
- 2018
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891. ; 36:2
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Tidskriftsartikel (refereegranskat)abstract
- The use of different natural and/or synthetic preparations ofCannabis sativais associated with therapeutic strategies for many diseases. Indeed, thanks to the widespread diffusion of the cannabinoidergic system in the brain and in the peripheral districts, its stimulation, or inhibition, regulates many pathophysiological phenomena. In particular, central activation of the cannabinoidergic system modulates the limbic and mesolimbic response which leads to food craving. Moreover, cannabinoid agonists are able to reduce inflammatory response. In this review a brief history of cannabinoids and the protagonists of the endocannabinoidergic system, i.e. synthesis and degradation enzymes and main receptors, will be described. Furthermore, the pharmacological effects of cannabinoids will be outlined. An overview of the involvement of the endocannabinoidergic system in neuroinflammatory and metabolic pathologies will be made. Finally, particular attention will also be given to the new pharmacological entities acting on the two main receptors, cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2), with particular focus on the neuroinflammatory and metabolic mechanisms involved.
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| 7. |
- Sivik, Tove, et al.
(författare)
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A validated and rapid high-performance liquidchromatography method for the quantification ofconversion of radio-labelled sex steroids
- 2010
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Ingår i: Hormone Molecular Biology and Clinical Investigation. - : de Gruyter. - 1868-1891. ; 3:1, s. 375-381
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Tidskriftsartikel (refereegranskat)abstract
- The 17b -hydroxysteroid dehydrogenase enzymes modify the availability of potent sex steroids and have thus attracted interest in the study of several steroid-dependent pathologies including breast, endometrial and prostate cancers. An increased awareness of the importance of steroidogenic enzymes has brought forth a demand for efficient assays to study the effects of individual enzymes on steroid levels. Methods used for assessing steroid conversion are often laborious and frequently involve hazardous sample preparation steps. We developed and validated an optimised simple method for sample preparation of sex steroids using protein precipitation by the addition of zinc sulphate/sodium hydroxide. The interconversion of radio-labelled oestrogens and androgens was quantified using high-performance liquid chromatography separation of oestrone, oestradiol, androstenedione and testosterone followed by online radiometric flow scintillation analysis. The method, which can be applied for assessing, e.g., the efficacy of inhibitors of steroidogenic enzymes, was successfully used for evaluating oestrogenic interconversion in breast cancer cell lines MCF7 and T-47D.
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| 8. |
- Söderqvist, G, et al.
(författare)
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Kjell Carlström (1940-2018)
- 2018
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Ingår i: Hormone molecular biology and clinical investigation. - : Walter de Gruyter GmbH. - 1868-1891. ; 35:1
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Tidskriftsartikel (refereegranskat)
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| 9. |
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