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Combination of factors | Combination of factors | ||
*[[Insulin]] deficiency | *[[Insulin]] deficiency | ||
*Development of relative insulin resistance | *Development of relative insulin resistance <ref name="pmid7555498">{{cite journal| author=Chen KW, Boyko EJ, Bergstrom RW, Leonetti DL, Newell-Morris L, Wahl PW | display-authors=etal| title=Earlier appearance of impaired insulin secretion than of visceral adiposity in the pathogenesis of NIDDM. 5-Year follow-up of initially nondiabetic Japanese-American men. | journal=Diabetes Care | year= 1995 | volume= 18 | issue= 6 | pages= 747-53 | pmid=7555498 | doi=10.2337/diacare.18.6.747 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7555498 }} </ref> | ||
===Insulin resistance=== | ===Insulin resistance=== | ||
Insulin resistance may be due to an inherent [[genetic]] risk factor. Insulin resistance may become more severe with increasing weight and age. It results in impaired glucose tolerance and overt [[hyperglycemia]]. Overt hyperglycemia may itself result in a toxic effect on beta cells by decreasing insulin [[gene expression]]. | Insulin resistance may be due to an inherent [[genetic]] risk factor. Insulin resistance may become more severe with increasing weight and age. It results in impaired glucose tolerance and overt [[hyperglycemia]]. Overt hyperglycemia may itself result in a toxic effect on beta cells by decreasing insulin [[gene expression]]. | ||
< | <ref name="pmid9022089">{{cite journal| author=Moran A, Zhang HJ, Olson LK, Harmon JS, Poitout V, Robertson RP| title=Differentiation of glucose toxicity from beta cell exhaustion during the evolution of defective insulin gene expression in the pancreatic islet cell line, HIT-T15. | journal=J Clin Invest | year= 1997 | volume= 99 | issue= 3 | pages= 534-9 | pmid=9022089 | doi=10.1172/JCI119190 | pmc=507829 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9022089 }} </ref> | ||
Revision as of 21:11, 25 May 2020
Synonyms and keywords: Diabetes; Diabetes insipidus; Diabetes insipidus; Congenital nephrogenic Diabetes insipidus; Cranial Diabetes insipidus; nephrogenic Diabetes insipidus; non-nephrogenic Diabetes insipidus; renal Diabetes mellitus type 1
Definition
Diabetes mellitus is a metabolic disease that results in dysregulation of blood sugar in the body.
Types
- Type 1 Diabetes Mellitus
- Type 2 Diabetes Mellitus
Type 1 Diabetes Mellitus
- Sudden onset
- Age: Any age, but mostly young
- ketoacidosis common
- Endogenous insulin low or absent
Type 2 Diabetes mellitus
- Gradual onset
- Age: Mostly adults
- May occur in younger individuals
- Ketoacidosis rare
- Endogenous insulin may be
- normal
- increased or
- decreased
Symptoms
- Diabetes mellitus is usually asymptomatic.
- Symptoms of Diabetes may include the following:
Pathophysiology
Combination of factors
Insulin resistance
Insulin resistance may be due to an inherent genetic risk factor. Insulin resistance may become more severe with increasing weight and age. It results in impaired glucose tolerance and overt hyperglycemia. Overt hyperglycemia may itself result in a toxic effect on beta cells by decreasing insulin gene expression. [2]
- ↑ Chen KW, Boyko EJ, Bergstrom RW, Leonetti DL, Newell-Morris L, Wahl PW; et al. (1995). "Earlier appearance of impaired insulin secretion than of visceral adiposity in the pathogenesis of NIDDM. 5-Year follow-up of initially nondiabetic Japanese-American men". Diabetes Care. 18 (6): 747–53. doi:10.2337/diacare.18.6.747. PMID 7555498.
- ↑ Moran A, Zhang HJ, Olson LK, Harmon JS, Poitout V, Robertson RP (1997). "Differentiation of glucose toxicity from beta cell exhaustion during the evolution of defective insulin gene expression in the pancreatic islet cell line, HIT-T15". J Clin Invest. 99 (3): 534–9. doi:10.1172/JCI119190. PMC 507829. PMID 9022089.