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- Tengholm, Anders, et al.
(author)
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Spatio-Temporal Dynamics of Phosphatidylinositol-3,4,5-Trisphosphate Signalling
- 2009
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In: Vitamines and Hormones. - 0083-6729. ; 80, s. 287-311
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Research review (peer-reviewed)abstract
- Many effects of insulin, insulin-like growth factors and other receptor stimuli are mediated via the phospholipid second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3). PIP3 is formed by the activity of phosphoinositide 3-kinases in the plasma membrane, where it serves to recruit signalling proteins. These proteins coordinate complex events leading to changes in cell metabolism, growth, movement and survival. Over the past decade, new techniques for measurements of PIP3 in the plasma membrane of individual living cells have markedly improved our understanding of the role of this messenger in a variety of cellular processes. This review summarises the mechanisms involved in formation and degradation of PIP3 in insulin-responsive cells, how PIP3 can be measured in individual cells as well as accumulating evidence that the plasma membrane PIP3 concentration undergoes complex spatiotemporal patterns in many types of cells, with particular emphasis on autocrine insulin-induced PIP3 oscillations in pancreatic beta-cells.
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- Ahrén, Bo, et al.
(author)
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Incretin hormone secretion over the day.
- 2010
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In: Vitamines and Hormones. - 0083-6729. ; 84, s. 203-220
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Journal article (peer-reviewed)abstract
- The two incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key factors in the regulation of islet function and glucose metabolism, and incretin-based therapy for type 2 diabetes has gained considerable interest during recent years. Regulation of incretin hormone secretion is less well characterized. The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. More recently, it has been established that a diurnal regulation exists with incretin hormone secretion to an identical meal being greater when the meal is served in the morning compared to in the afternoon. Finally, whether incretin hormone secretion is altered in disease states is an area with, so far, controversial results in different studies, although some studies have demonstrated reduced incretin hormone secretion in type 2 diabetes. This review summarizes our knowledge on regulation of incretin hormone secretion and its potential changes in disease states.
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- Hellström, Per M., 1954-
(author)
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Chapter Twelve – Glucagon-like peptide-1 : gastrointestinal regulatory role in metabolism and motility
- 2010
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In: Vitamines and Hormones. - 0083-6729. ; 84, s. 319-329
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Research review (peer-reviewed)abstract
- Gastrointestinal (GI) motility, primarily gastric emptying, balances the hormonal output that takes place after food intake in order to maintain stable blood sugar. The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), work together to reduce postprandial hyperglycemia by glucose-dependent insulin secretion and inhibition of glucagon release, as well as inhibition of GI motility and gastric emptying. GLP-1 is considered the more effective of the two incretins due to its additional inhibitory effects on GI motility. It is observed that patients on treatment with GLP-1 analogues or exenatide achieve a considerable weight loss during treatment. This is of benefit to improve insulin resistance in type 2 diabetes. Furthermore, weight loss per se is of considerable benefit in an even longer health perspective. The weight loss is considered to be due to the inhibition of GI motility. This effect has been studied in animal experimentation, and from there taken to involve studies on GI motility in healthy volunteers and patients with irritable bowel syndrome (IBS). Evolving to a phase II study in IBS, the GLP-1 analogue (ROSE-010) was recently shown to be effective for treatment of acute pain attacks in IBS. Taken together, data speak in favor of GI motility as a central component not only in metabolic disorders but also in IBS, be it due to a direct relaxing effect on GI smooth muscle or a slow emptying of gastric contents resulting in a less outspoken nutritional demand on hormonal regulatory functions in the GI tract.
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- Henning, Petra, 1974, et al.
(author)
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Stimulation of osteoclast formation and bone resorption by glucocorticoids: Synergistic interactions with the calcium regulating hormones parathyroid hormone and 1,25(OH)2-vitamin D3
- 2022
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In: Vitamins and Hormones Vol 120 Parathyroid Hormone. - : Elsevier. - 0083-6729. ; , s. 231-270
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Book chapter (other academic/artistic)abstract
- Osteoporosis is a significant health problem, with skeletal fractures increasing morbidity and mortality. Excess glucocorticoids (GC) represents the leading cause of secondary osteoporosis. The first phase of glucocorticoid-induced osteoporosis is increased bone resorption. In this Chapter, in vitro studies of the direct glucocorticoid receptor (GR) mediated cellular effects of GC on osteoclasts to affect bone resorption and indirect effects on osteoblast lineage cells to increase the RANKL/OPG ratio and stimulate osteoclastogenesis and bone resorption are reviewed in detail, together with detailed descriptions of in vivo effects of GC in different portions of the skeleton in research animals and humans. Brief sections are devoted to contrasting functions of GC in osteonecrosis, vitamin D formation, in vitro and in vivo bone resorptive actions dependent on vitamin D receptor and vitamin D toxicity, as well as the molecular basis of GR action. Included are also more detailed assessments of the interactions of GC with the major calcium regulating hormones, 1,25(OH)2-vitamin D3 and parathyroid hormone, describing the in vitro increases in RANKL/OPG ratios, osteoclastogenesis and synergistic bone resorption that occurs when GC is combined with either 1,25(OH)2-vitamin D3 or parathyroid hormone. Additionally, a molecular basic for the synergistic interaction of GC with 1,25(OH)2-vitamin D3 is provided along with a suggested molecular basic for the interaction between GC and parathyroid hormone.
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