| 1. |
- Mårtensson, Ulrika, et al.
(författare)
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Deletion of the G protein-coupled receptor 30 impairs glucose tolerance, reduces bone growth, increases blood pressure, and eliminates estradiol-stimulated insulin release in female mice.
- 2009
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Ingår i: Endocrinology. - : The Endocrine Society. - 1945-7170 .- 0013-7227. ; 150:2, s. 687-98
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Tidskriftsartikel (refereegranskat)abstract
- In vitro studies suggest that the G protein-coupled receptor (GPR) 30 is a functional estrogen receptor. However, the physiological role of GPR30 in vivo is unknown, and it remains to be determined whether GPR30 is an estrogen receptor also in vivo. To this end, we studied the effects of disrupting the GPR30 gene in female and male mice. Female GPR30((-/-)) mice had hyperglycemia and impaired glucose tolerance, reduced body growth, increased blood pressure, and reduced serum IGF-I levels. The reduced growth correlated with a proportional decrease in skeletal development. The elevated blood pressure was associated with an increased vascular resistance manifested as an increased media to lumen ratio of the resistance arteries. The hyperglycemia and impaired glucose tolerance in vivo were associated with decreased insulin expression and release in vivo and in vitro in isolated pancreatic islets. GPR30 is expressed in islets, and GPR30 deletion abolished estradiol-stimulated insulin release both in vivo in ovariectomized adult mice and in vitro in isolated islets. Our findings show that GPR30 is important for several metabolic functions in female mice, including estradiol-stimulated insulin release.
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| 2. |
- Santesson, Sabina, et al.
(författare)
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Airborne Single Cell Chemistry
- 2002
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Ingår i: European Biotechnology News. ; 1:1, s. 39-40
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Tidskriftsartikel (populärvet., debatt m.m.)
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| 3. |
- Dybjer, E., et al.
(författare)
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Incretin hormones, insulin, glucagon and advanced glycation end products in relation to cognitive function in older people with and without diabetes, a population-based study
- 2020
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Ingår i: Diabetic Medicine. - : Wiley. - 0742-3071 .- 1464-5491. ; 37:7, s. 1157-1166
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Tidskriftsartikel (refereegranskat)abstract
- Aim The aim of this observational study was to investigate relationships between physiological levels of glucometabolic biomarkers and cognitive test results in a population-based setting. Methods Cross-sectional data were obtained from the Swedish population-based Malmo Diet and Cancer Study Re-examination 2007-2012 comprising 3001 older people (mean age 72 years). Through oral glucose tolerance testing (OGTT), fasting and post-load levels of serum insulin, plasma glucagon, serum glucose-dependent insulinotropic peptide (GIP) and plasma glucagon-like peptide-1 (GLP-1) were measured. Insulin resistance and insulin sensitivity levels were calculated. In 454 participants, advanced glycation end products (AGEs) were estimated through skin autofluorescence. Associations between biomarkers and two cognitive tests, the Mini-Mental State Examination (MMSE) and A Quick Test of Cognitive Speed (AQT) respectively, were explored in multiple regression analyses. Results Positive associations following adjustments for known prognostic factors were found between MMSE scores and insulin sensitivity (B = 0.822, P = 0.004), 2-h plasma glucagon (B = 0.596, P = 0.026), 2-h serum GIP (B = 0.581, P = 0.040) and 2-h plasma GLP-1 (B = 0.585, P = 0.038), whereas negative associations were found between MMSE scores and insulin resistance (B = -0.734, P = 0.006), fasting plasma GLP-1 (B = -0.544, P = 0.033) and AGEs (B = -1.459, P = 0.030) were found. Conclusions Higher levels of insulin sensitivity, GIP and GLP-1 were associated with better cognitive outcomes, but AGEs were associated with worse outcomes, supporting evidence from preclinical studies. Glucagon was linked to better outcomes, which could possibly reflect neuroprotective properties similar to the related biomarker GLP-1 which has similar intracellular properties. Longitudinal and interventional studies are needed to further evaluate neuromodulating effects of these biomarkers. presented at the European Association for the Study of Diabetes (EASD) 2019, Barcelona, Spain
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| 4. |
- Islam, M. Shahidul, et al.
(författare)
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Interaction with the inositol 1,4,5-trisphosphate receptor promotes Ca2+ sequestration in permeabilised insulin-secreting cells
- 1991
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Ingår i: FEBS Letters. - 0014-5793 .- 1873-3468. ; 288:1-2, s. 27-29
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Tidskriftsartikel (refereegranskat)abstract
- Electropermeabilised insulin-secreting RINm5F cells sequestered Ca2+, resulting in a steady-state level of the ambient free Ca2+ concentration corresponding to 723 +/- 127 nM (mean +/- SEM, n = 10), as monitored by a Ca(2+)-selective minielectrode. Inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) promoted a rapid and pronounced release of Ca2+. This Ca2+ was resequestered and a new steady-state Ca2+ level was attained, which was always lower (460 +/- 102 nM, n = 10, P less than 0.001) than the steady-state Ca2+ level maintained before the addition of Ins(1,4,5)P3. Whereas the initial reuptake of Ca2+ subsequent to Ins(1,4,5)P3 stimulation was relatively slow, the later part of reuptake was fast as compared to the reuptake phases of a pulse addition of extraneous Ca2+. In the latter case the uptake of Ca2+ resulted in a steady-state level similar to that found in the absence of Ins(1,4,5)P3. Addition of Ins(1,4,5)P3 under this condition resulted in a further Ca2+ uptake and thus a lower steady-state Ca2+ level. Heparin, which binds to the Ins(1,4,5)P3 receptor, also lowered the steady-state free Ca2+ concentration. In contrast to Ins(1,4,5)P3, inositol 1,3,4,5-tetrakisphosphate was without effect on Ca2+ sequestration. These findings are consistent with the presence of a high-affinity Ins(1,4,5)P3 receptor promoting continuous release of Ca2+ under basal conditions and/or the Ins(1,4,5)P3 receptor being actively involved in Ca2+ sequestration.
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| 5. |
- Santesson, Sabina, et al.
(författare)
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Cell-cell communication between adipocytes and pancreatic beta-cells in acoustically levitated droplets
- 2009
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Ingår i: Integrative Biology. - : Oxford University Press (OUP). - 1757-9708 .- 1757-9694. ; 1:10, s. 595-601
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Tidskriftsartikel (refereegranskat)abstract
- Dysfunctional adipocytes and insulin-producing pancreatic beta-cells are hallmarks of human Type 2 diabetes and play important roles in the onset and progression of the disease. However, the precise mechanisms involved are complex and only partially understood. Here we present a new and unique method to perform single-cell and cell-cell communication studies in Type 2 diabetes-related research. The airborne analytical system offers "contactless'' sample handling in the sub-microlitre volume range and is here equipped with fluorescence imaging detection. The system utilizes acoustically levitated droplets as "wall-less'' test tubes and in-house constructed piezoelectric flow-through picolitre droplet dispensers for precise reagent supply. Hormone-mediated regulation of adipocyte lipolysis and communication between adipocytes and b-cells can be studied at the few-cell level. Thus, lipolysis could be detected in single adipocytes, whether it was induced by isoprenaline or inhibited by insulin. Furthermore, the airborne system allowed the comparison of lipolysis in adipocytes of different sizes: a large adipocyte responded more slowly than a small cell. Furthermore, stimulation of insulin secretion by high glucose or acetylcholine administration to a levitated drop containing insulin-producing b-cells resulted in inhibition of isoprenaline-induced lipolysis in adipocytes present in the same drop. The results show the applicability of the airborne analytical system for single cell analysis and for cell-cell communication studies as well as the potential for future analysis directly from human cells obtained from clinical biopsies.
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