Pancreatic islets rich in β cells and microdissected from noninbred ob/ob mice contained about 15 pmol sialic acid per μg dry weight as determined by a microversion of the Warren thiobarbituric acid method. Removal of half of the sialic acid by treatment with Clostridium perfringens neuraminidase had no effect on the islet content of insulin, moderately inhibited glucose oxidation, and resulted in

Glucose (20 mM) released insulin from pancreatic islets of C57BL 6J- db2J db2J mice, the response being potentiated by 1 mM 3-isobutyl-1-methylxanthine. Islets of C57BL KsJ- db db mice failed to respond to glucose and released only little insulin when challenged with both glucose and methylxanthine. After incubation with 0 or 20 mM glucose alone the islet content of adenosine 3′:5′-cyclic monophos

Chloromercuribenzene-p-sulphonic acid (0.1 mM) or 5,5′-dithiobis-(2-nitrobenzoic acid) (1 mM) alone had no effect on cyclic AMP in microdissected pancreatic islets of non-inbred ob/ob mice. In the presence of 1 mM 3-isobutyl-1-methylxanthine, the mercurial increased and the disulphide decreased the cyclic AMP content. Both sulphydryl reagents stimulated insulin release whether 3-isobutyl-1-methylx

Treatment of pancreatic islets from ob/ob-mice with bacterial neuraminidase (0.8 to 40 mU/ml) resulted in a significant decrease of the sialic acid content and of the secretory response to glucose. The inhibitory effect on the glucose stimulated insulin release was reproduced with different batches of neuraminidase from Clostridium perfringens and Vibrio cholera. Treatment with neuraminidase affec

Microdissected pancreatic islets of ob/ob mice were used to study whether glucose induced insulin release is associated with changes of the apparent extracellular space. Glucose at a concentration of 20 mM had no measurable effect on the islet uptake of sucrose and urea. In the presence of these space markers glucose stimulated insulin release significantly. The results do not invalidate the hypot

At a concentration of 1.0 mM, 6,6' dithiodinicotinic acid and 5,5' dithiobis (2 nitrobenzoic acid) stimulated insulin release from microdissected pancreatic islets of hereditary obese (ob/ob) mice. Microperifusion experiments showed that the secretory responses occurred promptly upon exposure to the sulfhydryl reagents. Perifusion with 6,6' dithiodinicotinic acid induced a sustained enhancement of

4-Acetamido-4′-isothiocyanostilbene-2,2′-disulphonic acid (SITS), an amino-reacting probe of plasma membranes, stimulated the release of insulin from micro-dissected pancreatic islets of ob/ob-mice. This effect of SITS was inhibited by adrenaline or by calcium deficiency. SITS did not inhibit the insulin-releasing action of glucose or leucine but rather potentiated the effect of glucose. In contra

The Swedish Parliament and Government has recently sanctioned a new 6 year undergraduate medical degree leading directly to license, followed by a 12 month introduction to work as a certified doctor. The undergraduate education is internationally harmonized and the 23 learning outcomes address competence needs in future Swedish and international health-care. Particular attention is given to profes

The uptake of chloromercuribenzene-p-sulphonic acid (CMBS) was studied in microdissected pancreatic islets of ob/ob-mice. After rapid initial binding, the uptake increased linearly with time, suggesting that CMBS diffused into the plasma membrane. The binding of CMBS was rapidly reversed on exposure to l-cysteine. Whereas glibenclamide had no effect, glucose and 4-acetamido-4′-isothiocyanostilbene

At a glucose concentration of 3mm or less, iodoacetamide had no effect on the release of insulin from microdissected pancreatic islets of ob/ob-mice. At higher glucose concentrations, iodoacetamide exerted both an initial stimulatory and a subsequent inhibitory action. When islets were perifused with 1mm-iodoacetamide and 17mm-glucose the inhibitory action predominated after about 15min of transie

Sulphur-containing analogues of d-glucose were tested for effects on insulin release, d-glucose transport and d-glucose oxidation in microdissected pancreatic islets of obese-hyperglycemic mice. Substituting sulphur for oxygen in the ring structure of d-glucose (5-thio-d-glucose) resulted in a total loss of insulin-releasing ability. 5-Thio-d-glucose inhibited d-glucose-stimulated insulin release,

The simultaneous release of insulin and glucagon was studied with isolated pancreas preparations from foetal and newborn mice. Glucose, alone or in combination with arginine, did not affect immunoreactive insulin (IRI) of glucagon-like immunoreactivity (GLI) release from the pancreases of 18-day-old foetal mice. However, on the first postnatal day, glucose stimulated the release of IRI and, in the

The effects of p-chloromercuribenzoic acid and chloromercuribenzene-p-sulphonic acid on pancreatic islets were studied in vitro. Obese–hyperglycaemic mice were used as the source of microdissected islets containing more than 90% β-cells. p-Chloromercuribenzoic acid and chloromercuribenzene-p-sulphonic acid stimulated insulin release at concentrations of 0.01mm or above. This stimulation was signif

To elucidate the role of biogenic amines in insulin secretion, pancreatic islets rich in β-cells were microdissected from obese-hyperglycemic mice and were incubated with 14C-labelled 5-hydroxytryptamine (5-HT). The saturability of uptake and the fact that 5-HT was accumulated to high levels indicated that the β-cells possess a transport system with great capacity for this amine. The initial uptak

Background: Carpal tunnel syndrome (CTS) is a common cause of pain, weakness, sensory loss, and activity limitations. Currently, the most common initial treatment is use of a rigid splint immobilizing the wrist, usually during night-Time, for several weeks. Evidence regarding the efficacy and effect durability of wrist splinting is weak. The treatment is associated with costs and may cause discomf

The effects of phlorizin on several parameters of β-cell function were studied with microdissected islets of obese-hyperglycemic mice. At a concentration of 10 mM, phlorizin significantly depressed insulin release, glucose transport, glucose oxidation, and the level of fructose 1,6-diphosphate, when tested in the presence of 10 mM glucose. Whereas 1 mM phlorizin inhibited glucose transport by abou