Positive alliesthesia after insulin.

Volunteers experienced sucrose solution as more pleasant 36-48 min after insulin, than after saline control. These changes in affective estimates correlate negatively with blood sugar at 30 min and positively at 50 min after the insulin injection.     

Effect of vagal denervation on insulin release after oral and intravenous glucose

Zusammenfassung Perorale Glykosebelastung ergab bei vagotomierten Ratten Erhöhung des Blutglykosespiegels. Nach intravenöser Glykosezufuhr wurden niedrigere Werte von immunoreaktivem Insulin im Serum gefunden. Ebenso war der insulinogene Index bedeutend niedriger sowohl nach peroraler als auch nach intravenöser Glykosezufuhr. Vagotomie dürfte somit die glykosebedingte Insulinfreisetzung reduzieren.     

Insulin secretion and (pro)insulin biosynthesis of cultured mice islets after glibenclamide loading in vitro

Summary Isolated islets from C57B1/6J mice exposed to 10 mmoles/1 glucose supplemented with 5 g/ml glibenclamide for 48 h released significantly less insulin in the subsequent short-time incubation thanuntreated controls (without glibenclamide), whereas insulin biosynthesis was not suppressed by glibenclamide treatment.Investigations were carried out as a part of the ForschungsprojektDiabetes mellitus und Fettstoffwechselstörungen, supported by the Ministry of Health of the GDR.     

Insulin secretion and (pro)insulin biosynthesis of cultured mice islets after glibenclamide loading in vitro

Isolated islets from C57Bl/6J mice exposed to 10 mmoles/l glucose supplemented with 5 micrograms/ml glibenclamide for 48 h released significantly less insulin in the subsequent short-time incubation than untreated controls (without glibenclamide), whereas insulin biosynthesis was not suppressed by glibenclamide treatment.     

Proinsulin C-peptide elicits disaggregation of insulin resulting in enhanced physiological insulin effects

Using surface plasmon resonance (SPR) and electrospray mass spectrometry (ESI-MS), proinsulin C-peptide was found to influence insulin-insulin interactions. In SPR with chip-bound insulin, C-peptide mixed with analyte insulin increased the binding, while alone C-peptide did not. A control peptide with the same residues in random sequence had little effect. In ESI-MS, C-peptide lowered the presence of insulin hexamer. The data suggest that C-peptide promotes insulin disaggregation. Insulin/insulin oligomer μM dissociation constants were determined. Compatible with these findings, type 1 diabetic patients receiving insulin and C-peptide developed 66% more stimulation of glucose metabolism than when given insulin alone. A role of C-peptide in promoting insulin disaggregation may be important physiologically during exocytosis of pancreatic β-cell secretory granulae and pharmacologically at insulin injection sites. It is compatible with the normal co-release of C-peptide and insulin and may contribute to the beneficial effect of C-peptide and insulin replacement in type 1 diabetics. Received 3 May 2006; received after revision 9 June 2006; accepted 12 June 2006 Free Online Access     

台风对浙江地区的正面影响

通过收集2003～2007年浙江副热带高压控制时期（6～10月）台风降水、大风及降温资料,应用统计分析的方法,阐述了台风登陆对浙江省内陆地区农业、工业和人民生活的影响,论证了台风对缓解浙江伏旱期间的干旱、提高农业产量、缓解用能压力、提高空气质量发挥的重要作用,提出了“台风-降水-大风受益链”。     

Regulation of insulin receptor function

Resistance to the biological actions of insulin contributes to the development of type 2 diabetes and risk of cardiovascular disease. A reduced biological response to insulin by tissues results from an impairment in the cascade of phosphorylation events within cells that regulate the activity of enzymes comprising the insulin signaling pathway. In most models of insulin resistance, there is evidence that this decrement in insulin signaling begins with either the activation or substrate kinase activity of the insulin receptor (IR), which is the only component of the pathway that is unique to insulin action. Activation of the IR can be impaired by post-translational modifications of the protein involving serine phosphorylation, or by binding to inhibiting proteins such as PC-1 or members of the SOCS or Grb protein families. The impact of these processes on the conformational changes and phosphorylation events required for full signaling activity, as well as the role of these mechanisms in human disease, is reviewed in this article. Received 3 August 2006; received after revision 1 December 2006; accepted 8 January 2007     

Positive and negative peptide signals control stomatal density

The stoma is a micro valve found on aerial plant organs that promotes gas exchange between the atmosphere and the plant body. Each stoma is formed by a strict cell lineage during the early stages of leaf development. Molecular genetics research using the model plant Arabidopsis has revealed the genes involved in stomatal differentiation. Cysteine-rich secretory peptides of the EPIDERMAL PATTERNING FACTOR-LIKE (EPFL) family play crucial roles as extracellular signaling factors. Stomatal development is orchestrated by the positive factor STOMAGEN/EPFL9 and the negative factors EPF1, EPF2, and CHALLAH/EPFL6 in combination with multiple receptors. EPF1 and EPF2 are produced in the stomatal lineage cells of the epidermis, whereas STOMAGEN and CHALLAH are derived from the inner tissues. These findings highlight the complex cell-to-cell and intertissue communications that regulate stomatal development. To optimize gas exchange, particularly the balance between the uptake of carbon dioxide (CO(2)) and loss of water, plants control stomatal activity in response to environmental conditions. The CO(2) level and light intensity influence stomatal density. Plants sense environmental cues in mature leaves and adjust the stomatal density of newly forming leaves, indicating the involvement of long-distance systemic signaling. This review summarizes recent research progress in the peptide signaling of stomatal development and discusses the evolutionary model of the signaling machinery.     

Effect of hyperkalemia on insulin secretion

Summary The effect of hyperkalemia on insulin secretion remains undefined. We evaluated portal and peripheral insulin levels in anesthetized dogs after infusions of KCl. The mean maximal increase in peripheral plasma potassium at infusion rates of 0.2 mEq/kg/h was 0.68±0.20 mEq/l. There were no significant increases in either portal or peripheral insulin levels. In contrast, in six dogs whose plasma potassium concentration increased in each case by more than 2.0 mEq/l (infusion rate of 0.5 mEq/kg/h), portal insulin levels increased fivefold (p<0.05). We conclude that only marked increases in plasma potassium concentration stimulate pancreatic insulin secretion.     

Effect of hyperkalemia on insulin secretion

The effect of hyperkalemia on insulin secretion remains undefined. We evaluated portal and peripheral insulin levels in anesthetized dogs after infusions of KCl. The mean maximal increase in peripheral plasma potassium at infusion rates of 0.2 mEq/kg/h was 0.68 +/- 0.20 mEq/l. There were no significant increases in either portal or peripheral insulin levels. In contrast, in six dogs whose plasma potassium concentration increased in each case by more than 2.0 mEq/l (infusion rate of 0.5 mEq/kg/h), portal insulin levels increased fivefold (p less than 0.05). We concluded that only marked increases in plasma potassium concentration stimulate pancreatic insulin secretion.