Last edited by Zulkihn
Monday, October 5, 2020 | History

2 edition of gastrointestinal stimulus to insulin secretion in lean and obese hyperglycaemic mice. found in the catalog.

gastrointestinal stimulus to insulin secretion in lean and obese hyperglycaemic mice.

Leonard Carl Best

gastrointestinal stimulus to insulin secretion in lean and obese hyperglycaemic mice.

by Leonard Carl Best

  • 77 Want to read
  • 18 Currently reading

Published by University of Aston in Birmingham. Department of Biological Sciences in Birmingham .
Written in English


Edition Notes

SeriesPh. D thesis
ID Numbers
Open LibraryOL19805452M

  Key Terms. insulin: A polypeptide hormone that regulates carbohydrate metabolism.; glycogen: A polysaccharide that is the main form of carbohydrate storage in animals and also converts to glucose as needed.; glucagon: A hormone, produced by the pancreas, that opposes the action of insulin by stimulating the production of sugar.; Glucagon and insulin are peptide hormones secreted by the.   How our nerves regulate insulin secretion Date: Decem Source: Karolinska Institutet Summary: Researchers have managed to graft beta cells into the eyes of mice .

Insulin is a hormone that helps control your body's blood sugar level and metabolism -- the process that turns the food you eat into energy. Your pancreas makes insulin and releases it into your. “The total rate of release of fat from fat tissue in people with obesity is higher than in lean people, not lower (11). Neither insulin nor anything else is trapping fat inside the fat tissue of people with obesity, making it hard to understand how obesity could be caused by this mechanism.” Most people with obesity are insulin resistant.

  Exogenous GLP‐1 infusion has been shown to normalise blood glucose concentrations and the overall glycaemic response, in both healthy volunteers and patients with type 2 diabetes. 79 This occurs as a result of stimulation of insulin secretion, suppression of glucagon release and slowing GE. 80, 81 Exogenous GLP‐1 slows GE substantially, and. Calcium-dependent Insulin Secretion; The final link which completes the connection between blood glucose concentration and insulin secretion is calcium-dependent exocytosis of insulin-containing secretory vesicles. The rate at which this exocytic process .


Share this book
You might also like
Postmark Australia

Postmark Australia

PRELIMINARY GEOLOGIC MAP OF THE MESQUITE QUADRANGLE, CLARK AND LINCOLN COUNTIES, NEVADA AND MOHAVE COUNTY, ARIZONA... USGS OFR

PRELIMINARY GEOLOGIC MAP OF THE MESQUITE QUADRANGLE, CLARK AND LINCOLN COUNTIES, NEVADA AND MOHAVE COUNTY, ARIZONA... USGS OFR

François Villon.

François Villon.

Justice in eighteenth-century Hackney

Justice in eighteenth-century Hackney

[New York City marathon].

[New York City marathon].

Means of Transportation

Means of Transportation

Language, media and the politics of representation in South Africa.

Language, media and the politics of representation in South Africa.

The eurhythmics of Jaques-Dalcroze

The eurhythmics of Jaques-Dalcroze

Guide to company law in Malaysia & Singapore.

Guide to company law in Malaysia & Singapore.

Delegates report

Delegates report

The classical guitar

The classical guitar

body

body

The new methodical, easy and complete Dene syllabary

The new methodical, easy and complete Dene syllabary

The works of Apuleuis

The works of Apuleuis

Gastrointestinal stimulus to insulin secretion in lean and obese hyperglycaemic mice by Leonard Carl Best Download PDF EPUB FB2

Abstract. The gastrointestinal stimulus to the release of insulin has been investigated in man by the use of a radioimmunoassay for secretin. Serum secretin levels rose rapidly after the oral ingestion of glucose or protein and preceded the elevation of serum by: solely on enhanced insulin secretion.

Secretin appears to have a dual role in insulin release, an early direct stimulation followed by a prolonged po-tentiation of the glycemic stimulus. The potentiating effect is of such magnitude to suggest that secretin is the dominant factor in the enteric component of insulin release after an oral glucose.

The effects of large-dose oral arginine administration on the secretion of insulin by islet β-cells in healthy adults were determined. Eight non-obese healthy volunteers with normal glucose tolerance participated randomly in tests with four stages (with an interval of at least 3 days): the ml purified water stage (PWS), the 75 g glucose stage (GSS), the 30 g arginine stage (ARS) and the Cited by: 2.

Diurnal variations in food consumption and plasma concentrations of glucose and insulin were determined at 3-hourly intervals in obese hyperglycaemic mice (C57BL/6J ob/ob) and lean mice. The high vagal stimulation of insulin secretion was previously reported in obese patients (47, 48) and in rodent models of T2D (fa/fa rats, preobese ob/ob mice, high fatfed mice, and mice.

insulin secretion in vitro and in vivo and discusses their clinical relevance. Introduction Insulin, which is secreted from pancreatic β cells, is the key hor-mone in regulating glucose metabolism.

Insulin secretion is a highly dynamic process regulated by complex mechanisms. Glucose tolerance after meal ingestion in vivo is the result of multiple processes that occur in parallel.

Insulin secretion together with reciprocal inhibition of glucagon secretion contributes to glucose tolerance. However, other factors beyond glucose effectiveness and insulin action require consideration.

The absorption of ingested nutrients and their subsequent systemic rate of appearance. Glucose is the principal regulator of insulin secretion from pancreatic beta cells in islets of Langerhans (1, 2); however, intra-islet communication through paracrine interactions may also exert an important level of control over insulin secretion and ultimately glucose example, glucagon secreted from islet alpha cells potentiates insulin secretion (), whereas somatostatin.

Gastrointestinal (GI) hormones act in concert with the nervous system to regulate exocrine and endocrine GI secretion, cell proliferation, differentiation, and motility. The GI tract produces many different peptide hormones and GI-active neuropeptides, some of which are listed in Tables 1 and 2.

A: Increased blood glucose concentrations B: increased blood calcium concentrations C: increased body temperature D: increased exposure to sunlight. Both OEA and AS enhanced insulin release and improved glucose tolerance in vivo in NIH Swiss mice.

These results demonstrate the cellular localisation of GPR on islet cells (β and pancreatic polypeptide cells), its activation of the β-cell stimulus-secretion coupling pathway and glucose lowering effects in vivo. Insulin Secretion. Insulin secretion stimulated by glucose is a complex process of signal transduction in beta cells, comprised of proximal events which include glucose internalization through glucose transporters (GLUT) and its catabolism through glycolysis, Krebs cycle, and oxidative phosphorylation, leading to a rise in ATP/ADP ratio, and by distal events, which include the activation of.

In high-fat-fed mice, even the partial impairment of GIP secretion induced by the truncation of the prepro-GIP gene alleviates obesity and insulin resistance (Nasteska et al.

There is, accordingly, a rationale for the use of diets that have little effect on GIP secretion for the prevention/management of obesity, fatty liver and insulin. Islet cells interact with each other through direct contact and through their products (e.g. glucagon stimulates insulin secretion and somatostatin inhibits insulin and glucagon secretion) (Figure ).

The blood flow within the islets is organized centrifugally so that the different cell types are supplied in the sequence β → α → δ. Glucose-stimulated insulin secretion.

At basal levels of blood glucose (left-hand panel), the ATP-sensitive K + channels (K ATP channels) in pancreatic β-cells remain open, maintaining membrane hyperpolarization, Ca 2+ channel closure and inhibiting insulin secretion.

A rise in blood glucose (right-hand panel) drives oxidative phosphorylation and ATP production, resulting in the. effects on insulin secretion bot,h upon, and independent of, the cyclic AMP system.

Cyclic adenosine 3’:5’-monophosphate is presumed to be an during glucose-induced insulin release (, 8, 9). Further important mediator of insulin secretion in the B cell of the data have implied that glucose and CAMP induce insulin.

About 10 liters of fluid pass through the gastrointestinal system each day, and only about 2 liters are ingested, the rest represent secretions from the system itself. About half,liters is secreted from the exocrine glands, the salivary glands, the stomach and the liver, the other half is secreted by the epithelial cells of the of the.

GIP --> insulin secretion (with glucose and aa) Physiological Stimuli for Gastrointestinal Hormone Secretion. S - stimulates I - inhibits. Physiological Actions of Gastrointestinal Hormones Site of secretion: Antral mucosal G cells + stimulus: GRP, acetylcholine, proteins and gut stretch.

Type 2 Diabetes Mellitus (T2DM), one of the most common metabolic disorders, is caused by a combination of two primary factors: defective insulin secretion by pancreatic β-cells and the inability of insulin-sensitive tissues to respond appropriately to insulin.

Because insulin release and activity are essential processes for glucose homeostasis, the molecular mechanisms involved in the. About half of insulin secretion occurs as basal insulin release, while the other half occurs as ‘bolus’ insulin responses to a meal (46).

This basal-bolus dynamic of insulin secretion is important in considering clinical management of the diabetic patient (Figure 4). In those with complete insulin deficiency—e.g.

type 1 diabetes, late. This phase of secretion normally accounts for about 20 percent of the gastric secretion associated with eating a meal. Key Terms. conditioned reflex: A response, to a stimulus, that has been acquired by operant conditioning. cephalic phase: This occurs before .The mechanism behind exercise-induced decreases in plasma insulin concentrations was examined in eight healthy young men.

In addition, the influence of specific α1- and α2-adrenoceptor blockade on glucose kinetics during exercise was studied. To test the hypothesis that exercise-induced decreases in insulin secretion are mediated via α2-adrenoceptors, all subjects exercised for 60 min on.

If the carbohydrates include glucose, then that glucose will be absorbed into the bloodstream and blood glucose level will begin to rise.

In target cells, insulin initiates a signal transduction, which has the effect of increasing glucose uptake and storage. Finally, insulin is degraded, terminating the response.