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Pancreatic secretion metabolic requirements

So far it has been implied that adaptation of homeostatic mechanisms within the limits of overload may be without risk in the short term, but the situation may be different when one considers chronic stress over a lifespan. Thus it has been claimed that overstimulation of pancreatic secretion of insulin by excessive consumption of sugar can lead to exhaustion of the homeostatic process, i.e. while adaptation can be sustained in the short term, ultimately the control breaks down and diabetes results. Hence the acute toxicity of sucrose is low and probably results from dehydration, whereas a completely different mechanism may apply to the chronic toxicity. Acute and short-term tests cannot give a complete picture of the consequences of metabolic overload, and chronic toxicity tests will continue to be required in the foreseeable future—and not merely to assess carcinogenic hazard. [Pg.177]


See other pages where Pancreatic secretion metabolic requirements is mentioned: [Pg.217]    [Pg.1728]    [Pg.116]    [Pg.141]    [Pg.625]    [Pg.997]    [Pg.625]    [Pg.336]    [Pg.303]    [Pg.303]    [Pg.336]    [Pg.195]    [Pg.181]    [Pg.177]    [Pg.155]    [Pg.537]    [Pg.538]    [Pg.543]   
See also in sourсe #XX -- [ Pg.445 , Pg.446 ]




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