Download PDF by David Leslie, Cecilia Lansang, Simon Coppack, Laurence: Diabetes : Clinician's Desk Reference

By David Leslie, Cecilia Lansang, Simon Coppack, Laurence Kennedy

ISBN-10: 184076158X

ISBN-13: 9781840761580

ISBN-10: 1840766174

ISBN-13: 9781840766172

The ebook explains the underlying pathophysiology of the affliction and covers intimately all its major varieties and problems. Separate chapters examine the variety of healing procedures, including summaries of key medical trials. insurance additionally contains epidemiology and category, in addition to prognosis, screening, restricting hazard, and different points of illness administration and sufferer care. The booklet is illustrated all through by way of explanatory diagrams, graphs, tables, and pictures.

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Peripheral VLDL-triglyceride clearance may be impaired because insulin is needed to synthesize and secrete lipoprotein lipase, the principal enzyme responsible for clearing VLDL-triglyceride in some tissues. ȣ Insulin also promotes LDL receptor function. v Poor glycemic control in type 1 diabetes is associated with high concentrations of VLDL-cholesterol, LDL-cholesterol and total triglycerides, and sometimes with low HDL-cholesterol. Adequate insulin therapy usually leads to a fall in total triglyceride, and abnormalities of VLDL and LDL also improve.

G. GLUT1, GLUT2) have been associated with inborn errors of carbohydrate metabolism. ȣ The insulin-sensitizing agents metformin and the thiazolidinediones appear to increase cell surface expression of GLUT4, as does physical exercise. v Glucose can be moved against a concentration gradient – necessary in the special circumstances of the renal tubule and intestinal epithelium – by using a family of at least three known sodium– glucose co-transporters (SGLTs). ȣ At least one of these co-transporters (SGLT3) appears to have some glucose concentrationsensing function.

In addition, they have growth-promoting effects mediated by two IGF receptors. v Insulin is a weak agonist of IGF receptors. Abnormalities of insulin synthesis and secretion v The most common abnormality is the progressive loss of normal pulsatility, delayed insulin response to hyperglycemia, and gradual loss of insulin secretory capacity seen as obese individuals move towards type 2 diabetes. The progressive loss of insulin secretion in type 1 diabetes has a different natural history. v However, there are also some rarer, genetic abnormalities of insulin structure involving mutations of the DNA code for insulin and hence altered amino acid sequences.

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Diabetes : Clinician's Desk Reference by David Leslie, Cecilia Lansang, Simon Coppack, Laurence Kennedy

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