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Beta-cells

Diabetes mellitus is a complicated, chronic disorder characterized by either insufficient insulin production by the beta cells of die pancreas or by cellular resistance to insulin. Insulin insufficiency results in elevated blood glucose levels, or hyperglycemia As a result of the disease, individuals with diabetes are at greater risk for a number of disorders, including myocardial infarction, cerebrovascular accident (stroke), blindness, kidney disease, and lower limb amputations. [Pg.487]

Insulin is a hormone manufactured by the beta cells of the pancreas. It is the principal hormone required for the proper use of glucose (carbohydrate) by the body. Insulin also controls the storage and utilization of amino acids and fatty acids. Insulin lowers blood glucose levels by inhibiting glucose production by the liver. [Pg.488]

The sulfonylureas appear to lower blood glucose by stimulating the beta cells of the pancreas to release insulin. The sulfonylureas are not effective if the beta cells of the pancreas are unable to release a sufficient amount of insulin to meet the individual s needs. The first generation sulfonylureas (eg, chlorpropamide, tolazamide, and tolbutamide) are not commonly used today because they have a long duration of action and a higher incidence of adverse... [Pg.499]

Like the sulfonylureas, the meglitinides act to lower blood glucose levels by stimulating the release of insulin from the pancreas. This action is dependent on the abilily of the beta cell in the pancreas to produce some insulin. However, the action of die meglitinides is more rapid than that of the sulfonylureas and their... [Pg.502]

Margulis, B.A., Sandler, S., Eizirik, D.L., Welsh, N., Welsh, M. (1991). Liposomal delivery of purified heat shock protein hsp70 in rat pancreatic islets as protection against interleukin I beta-induced impaired beta cell function. Diabetes 40, 1418-1422. [Pg.457]

Weber LM, Hayda KN, Haskins K et al (2007) The effects of cell-matrix interactions on encapsulated beta-cell function within hydrogels functionalized with matrix-derived adhesive... [Pg.167]

Newgard CB, McGarry JD Metabolic coupling factors in pancreatic beta-cell signal transduction. Annu Rev Biochem 1995 64 689. [Pg.162]

Immune complex enhancement. Beta-cells activation and Increased insulin production (Btuni, 1988). Neuro-regulatory effect (Nakazawa et al., 1977 Btuni, 1988 Hiraga et al., 1993). [Pg.355]

Regulation of fasting serum glucose, improvement of glucose utilization, improvement in energy. Beta-cells activation and enhancement of insuhn production (Sugano et al., 1984). [Pg.355]

Improvement of peripheral insulin utilization, beta-cells activation and increased insulin production. [Pg.355]

Rice bran is the richest natural source of B-complex vitamins. Considerable amounts of thiamin (Bl), riboflavin (B2), niacin (B3), pantothenic acid (B5) and pyridoxin (B6) are available in rice bran (Table 17.1). Thiamin (Bl) is central to carbohydrate metabolism and kreb s cycle function. Niacin (B3) also plays a key role in carbohydrate metabolism for the synthesis of GTF (Glucose Tolerance Factor). As a pre-cursor to NAD (nicotinamide adenine dinucleotide-oxidized form), it is an important metabolite concerned with intracellular energy production. It prevents the depletion of NAD in the pancreatic beta cells. It also promotes healthy cholesterol levels not only by decreasing LDL-C but also by improving HDL-C. It is the safest nutritional approach to normalizing cholesterol levels. Pyridoxine (B6) helps to regulate blood glucose levels, prevents peripheral neuropathy in diabetics and improves the immune function. [Pg.357]

More recently, free radicals have been postulated to mediate part of the beta cell cytotoxicity of interleukin-1 (IL-1), a peptide hormone produced by macrophages. [Pg.187]

Taken together, these observations emphasize the critical importance of maintaining the antioxidant potential of the pancreatic beta cell in ordet to ensure both its survival and insulin secretory capacity during times of increased oxidative stress. [Pg.187]

Prevention of vascular disease is one of the goals of a study in progress in Sweden, in which newly diagnosed diabetic children have been randomized in a doubleblind study where one group receives placebo and the other a preparation containing ascorbic acid, )3-carotene, nicotinamide, selenium and vitamin E (Ludvigsson, 1992). Future research with antioxidants may attempt to prevent the onset of pancreatic beta-cell destruction in the prediabetic phase of susceptible individuals. [Pg.193]

N9. Nishi, S Stoffel, M., Xiang, K Shows, T. B Bell, G. I., and Takeda, J Human pancreatic beta-cell glucokinase cDNA sequence and localization of the polymorphic gene to chromosome 7, band p 13. Diabetologia 35,743-747 (1992). [Pg.48]

Insulin mRNA splicing rates were estimated from the rate of disappearance of the insulin preRNA signal from beta-cells treated with actinomycin D to block transcription. The two introns in mouse insulin II are not spliced with the same ef-... [Pg.230]

At least two classes of regulated secretion can be defined [54]. The standard regulated secretion pathway is common to all secretory cells (i.e. adrenal chromaffin cells, pancreatic beta cells, etc.) and works on a time scale of minutes or even longer in terms of both secretory response to a stimulus and reuptake of membranes after secretion. The second, much faster, neuron-specific form of regulated secretion is release of neurotransmitters at the synapse. Release of neurotransmitters may occur within fractions of a second after a stimulus and reuptake is on the order of seconds. Indeed, synaptic vesicles may be recycled and ready for another round of neurotransmitter release within 1-2 minutes [64]. These two classes of regulated secretion will be discussed separately after a consideration of secretory vesicle biogenesis. [Pg.154]

Graves, P.M., etal. Prospective study of enteroviral infections and development of beta-cell autoimmunity. Diabetes autoimmunity study in the young (DAISY), Diabetes Res. Clin. [Pg.449]

Does nitric oxide mediate autoimmune destmction of beta-cells Possible therapeutic interventions in IDDM, Diabetes 41 (1992), p. 897-903... [Pg.277]


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See also in sourсe #XX -- [ Pg.60 , Pg.61 ]

See also in sourсe #XX -- [ Pg.61 , Pg.63 ]

See also in sourсe #XX -- [ Pg.359 ]




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