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P Khalid

Publications and source records attributed to P Khalid.

7 recordsLinked to original sources
PubMed1991

The role of ATP and free ADP in metabolic coupling during fuel-stimulated insulin release from islet beta-cells in the isolated perfused rat pancreas.

The isolated perfused rat pancreas was used to test the hypothesis that total cellular ATP or the ratio of ATP/free ADP plays the primary role in coupling intermediary metabolism to the biophysical events that are the basis of glucose-stimulated insulin release. The pancreas was preperfused for 20 min with 4.0 mM of a physiological mixture of 20 amino acids plus 4.2 mM glucose, and insulin release was then stimulated for 150 s by suddenly increasing the glucose to 8.3 mM. The pancreas was sampled at 24, 48, 72, and 150 s after the switch. The content of total ATP, ADP, AMP, Pi, phosphocreatine, and creatine were measured in beta-cell enriched cores of pancreatic islets microdissected from freeze-dried pancreas cryostat sections. Metabolites were measured by quantitative histochemical enzymatic cycling techniques. Modeling studies were carried out to assess the impact of biochemical analytical results on the membrane potential of the beta-cells. The level of free ADP was calculated using the creatine kinase equilibrium reaction and an intracellular pH of 7.2. First phase insulin release was stimulated at least 10-fold with the maximum reached 45 s after adding high glucose. The biochemical analytical data demonstrate that the total cellular level of the putative coupling factor ATP and of the ratios ATP/free ADP and ATP/free ADP x Pi are not significantly influenced by a glucose level change that causes a more than 10-fold surge of insulin release. The strength and limitations of the present experimental strategy and the implications of the results for our understanding of metabolic coupling in glucose-stimulated insulin release are discussed.

Adenosine Diphosphate↗
PubMed1991

Effect of linogliride on hormone release from perfused rat pancreas. Fuel dependence and desensitization by tolbutamide.

We examined the effect of the hypoglycemic drug linogliride on hormone release from the in vitro perfused rat pancreas. Linogliride stimulated insulin release in the absence of glucose either in the presence or absence of a physiological mixture of amino acids. In addition, linogliride inhibited amino acid-induced glucagon release. Half-maximal effects of linogliride on insulin and glucagon release were achieved at concentrations as low as 26 and 3 microM, respectively. The effects of linogliride on hormone release largely resembled those of tolbutamide. In the absence of amino acids, the stimulation of insulin release by linogliride or tolbutamide was transient. When the pancreas had been preperfused for 20 min with tolbutamide, linogliride no longer had an effect on hormone release. Likewise, tolbutamide remained without effect in pancreases preperfused with linogliride. These data suggest that linogliride and tolbutamide may have a similar mechanism of action.

Amino Acids↗
PubMedDate not supplied

Effect of age on the binding of lectin 125I-PHA-B to pancreatic islets of rat in vitro and stimulation of some cellular events.

Agaricus bisporus lectin (PHA-B) stimulates insulin release in vitro. The stimulation is associated with increased conversion of proinsulin to insulin in the isolated islets of Langerhans of rats. Both these functions are directly proportional to the binding of I125 PHA-B, which is more marked in the islets from younger rats. The lectin binding to islets is not affected by glucose concentration in the medium.

Agaricus↗
PubMedDate not supplied

Effect of some novel synthetic analogues of CCK-4 on insulin and glucagon secretion.

The biologic activities of three synthetic analogues of CCK-4 (Trp-Met-Asp-Phe-NH2) in which (i) the C-terminal residue Phe was N-methylated (peptide I); (ii) the C-terminal Phe residue was N-methylated and Ser is substituted for Met in position 2 (peptide II); (iii) Pro was substituted for Trp in position 1 and the C-terminal amino nitrogen was methylated (peptide III), have been described. Peptides I and II have been found to inhibit the release of both insulin and glucagon, while peptide III was found to be a potent releasing agent for insulin and an inhibitor for glucagon.

Amino Acid Sequence↗
PubMedDate not supplied

Insulin like activity in (-) epicatechin.

Water extract of the bark of plant of Pterocarpus marsupium Roxb is used as an antidiabetic drug in indigenous medicine in India. (-) Epicatechin, its active principle, has been found to be insulinogenic. The present in vitro study reports some insulin like activities of (-) epicatechin. Like insulin, (-) epicatechin stimulates oxygen uptake in fat cells and tissue slices of various organs, increases glycogen content of rat diaphragm in dose-dependent manner with corresponding increase in U14-C glucose uptake, and inhibits theophylline induced lipolysis in isolated fat pads in dose-dependent manner. Experiments on competitive binding of 125I-insulin and (-) epicatechin to liver cell plasma membrane indicate that insulin does not share binding site with (-) epicatechin. (-) Epicatechin at a concentration of up to 1 mM does not effect the release of glucagon from the islets in vitro. Thus, (-) epicatechin has insulinogenic as well as insulin like properties.

Adipose Tissue↗
PubMedDate not supplied

Synthetic analogs of cholecystokinin terminal tetrapeptide that stimulate insulin but not glucagon release from pancreatic islets.

Two synthetic analogs of CCK-4, Glp-Met-Asp-Phe-NH2 (I) and Pro-Met-Asp-Phe-NH2 (II) reported earlier to stimulate insulin release from the isolated rat pancreatic islets in vitro at concentrations as low as 10(-10) M, have now been found to be totally ineffective as glucagon releasers at concentrations as high as 10(-6) M or higher. It is evident that the replacement of Trp in CCK-4 by Glp and Pro residues leads to peptides which exhibit insulin releasing activity without stimulating the release of glucagon.

Animals↗