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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
An in vitro system with microdissected mouse islets was employed for studying insulin release. Islets from obese-hyperglycemic mice were considered particularly useful in view of their high content of adequately functioning β-cells. After freeze-drying and weighing each of the incubated islets it was possible to express the rate of insulin release per islet dry weight. Insulin released from a sing
The insulin-releasing ability and uptake characteristics of non-metabolizable, transport-specific amino acids were studied in an in vitro system, using microdissected pancreatic islets with more than 90% β-cells. Among the four stereoisomers of 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid (BCH), only the b(-) form stimulated insulin release. This isomer is known as a specific substrate for trans
The limiting factor for quantitative histochemistry employing freeze-dried tissue sections is the ability to identify morphologic structures. Satisfactory staining of freeze-dried tissue specimens intended for further microanalysis was achieved by using isopentane solutions of free dye bases. The practical details of this rapid histologic control are outlined and its usefulness is illustrated by m
Previous studies have revealed the existence of two separate phases in the glucose-stimulated insulin release. Exposure of microdissected mouse islets to mannoheptulose or epinephrine effectively inhibited both the initial transient release and the second persistent phase of insulin secretion. These results suggest that metabolism of glucose is a prerequisite for both phases of insulin release. Th
The pancreatic islets in obese-hyperglycemic mice display a normal response of insulin secretion when stimulated with glucose in vitro. This indicates that the impaired glucose metabolism is due to extra-pancreatic factors rather than to deficient β-cell function. In fact, the pancreas of these mice is a useful source from which to isolate large numbers of mammalian β-cells suitable for studies of
