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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

J type diabetes is grouped as a subtype of type III or malnutrition-related diabetes, known as protein-deficient pancreatic diabetes, (PDPD). J type diabetes has not been reported recently, but a clinical picture called phasic insulin-dependent diabetes mellitus (PIDDM) has been elaborated in Jamaica, the same home country of PDRD and appears to be a "formes frustes" syndrome. The following comparative studies were performed on a group of diabetic patients and normal controls: insulin receptor binding; renal, hepatic, and pancreatic function; and abdominal ultrasonography. The results show a considerably decreased white and red blood cell binding to insulin (P less than .05), extensive kidney damage (P less than .05), and increased pancreatic echogenicity in PIDDM, supporting a separate identity of this latter syndrome from types I and II diabetes mellitus. Also, the features of relative insulin resistance, absence of ketosis even in the presence of severe hyperglycemia, and intermittent insulin requirement suggests that PIDDM, J type diabetes, and PDPD are one and the same syndrome.
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PMID:J type diabetes revisited. 162 24

The global epidemic of diabetes has extended to the developing countries including Sub-Sahara Africa. In this context, blacks with type 2 diabetes in the African Diaspora continue to manifest 1.5-2 times higher prevalent rates than in their white counterparts. Previous studies have demonstrated that blacks with and without type 2 diabetes have alterations in hepatic and peripheral insulin sensitivity, beta-cell function, and hepatic insulin clearance as well as hepatic glucose dysregulation when compared to whites. In addition, non-diabetic blacks in the African Diaspora manifest multiple metabolic mediators that predict type 2 diabetes and its subtypes. These pathogenic modifiers include differences in subclinical inflammation, oxidative stress burden, and adipocytokines in blacks in the African Diaspora prior to clinical diagnosis. Consequently, blacks in the African Diaspora manifest subtypes of type 2 diabetes, including ketosis-prone diabetes and J type diabetes. Given the diversity of type 2 diabetes in blacks in the African Diaspora, we hypothesize that blacks manifest multiple early pathogenic defects prior to the diagnosis of type 2 diabetes and its subtypes. These metabolic alterations have strong genetic component, which appears to play pivotal and primary role in the pathogenesis of type 2 diabetes and its subtypes in blacks in the African Diaspora. However, environmental factors must also be considered as major contributors to the higher prevalence of type 2 diabetes and its subtypes in blacks in the African Diaspora. These multiple alterations should be targets for early prevention of type 2 diabetes in blacks in the African Diaspora.
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PMID:Racial Disparities in the Pathogenesis of Type 2 Diabetes and its Subtypes in the African Diaspora: A New Paradigm. 2689 11