scholarly journals Genetic, metabolic and clinical characteristics of maturity onset diabetes of the young

1998 ◽  
pp. 233-239 ◽  
Author(s):  
G Velho ◽  
P Froguel
Keyword(s):  
Late Onset ◽  
Microvascular Complications ◽  
Pancreatic Beta Cell ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Minor Role ◽  
Hepatic Glycogen ◽  
Maturity Onset Diabetes ◽  
Primary Defect ◽  
Onset Diabetes

Maturity onset diabetes of the young (MODY) is a genetically and clinically heterogeneous subtype of non-insulin-dependent diabetes mellitus (NIDDM) characterised by early onset, autosomal dominant inheritance and a primary defect in insulin secretion. To date, three MODY genes have been identified on chromosomes 20q (MODY1/hepatic nuclear factor (HNF)-4alpha), 7p (MODY2/glucokinase) and 12q (MODY3/HNF-1alpha). Mutations in MODY2/glucokinase result in mild chronic hyperglycaemia as a result of reduced pancreatic beta-cell responsiveness to glucose, and decreased net accumulation of hepatic glycogen and increased hepatic gluconeogenesis after meals. In contrast, MODY1 and MODY3 are characterised by severe insulin secretory defects, and by major hyperglycaemia associated with microvascular complications. The role of the three known MODY genes in susceptibility to the more common late-onset NIDDM remain uncertain. Genetic studies seem to exclude a role as major susceptibility genes, but leave unresolved whether they may have a minor role in a polygenic context or an important role in particular populations.

scholarly journals Pancreatic beta cell protection/regeneration with phytotherapy

2015 ◽  
Vol 51 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Azar Hosseini ◽  
Reza Shafiee-Nick ◽  
Ahmad Ghorbani
Keyword(s):  
Beta Cell ◽  
Late Onset ◽  
Pancreatic Beta Cell ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Cell Protection ◽  
Cell Degeneration ◽  
Number Of Patients ◽  
Insulin Dependent ◽  
Beta Cell Protection

Although currently available drugs are useful in controlling early onset complications of diabetes, serious late onset complications appear in a large number of patients. Considering the physiopathology of diabetes, preventing beta cell degeneration and stimulating the endogenous regeneration of islets will be essential approaches for the treatment of insulin-dependent diabetes mellitus. The current review focused on phytochemicals, the antidiabetic effect of which has been proved by pancreatic beta cell protection/regeneration. Among the hundreds of plants that have been investigated for diabetes, a small fraction has shown the regenerative property and was described in this paper. Processes of pancreatic beta cell degeneration and regeneration were described. Also, the proposed mechanisms for the protective/regenerative effects of such phytochemicals and their potential side effects were discussed.

Clinical features, lifestyle management, and glycaemic targets in type 2 diabetes mellitus

2011 ◽  
pp. 1774-1779
Author(s):  
David Matthews ◽  
Usha Ayyagari ◽  
Pamela Dyson
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Urban Communities ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Maturity Onset Diabetes ◽  
Onset Diabetes ◽  
The Usa ◽  
High Level

Type 2 diabetes—previously named ‘maturity-onset diabetes’ or ‘non-insulin-dependent diabetes mellitus’—was, in the past, generally diagnosed in individuals over the age of 40 years old, but, with the modern epidemic, is found in increasing numbers in younger people, including teenagers and children. It is strongly associated with overweight and obese individuals, and tends to run in families. This feature may be environmental, since being overweight also runs in families, but there are specific genes for obesity (1). Type 2 diabetes that occurs in younger individuals with a very strong family history of early-onset diabetes may be the autosomally dominant ‘maturity-onset diabetes of the young’ (MODY) (see Chapter 13.3.4). In an environment where there is a pandemic of diabetes, one should maintain a very high level of suspicion of diabetes in those who are overweight—in the USA, the prevalence of type 2 diabetes is running at 8% of the population, and, in South India and Sri Lanka, at up to 18% in urban communities (2).

Maturity-Onset Diabetes of the Young: Recent Findings Indicate Insulin Resistance/Obesity Are Not Factors

1998 ◽  
Vol 24 (4) ◽  
pp. 477-480
Author(s):  
E. Ann Cabanas
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cell Function ◽  
Age Of Onset ◽  
Pancreatic Beta Cell ◽  
Maturity Onset Diabetes ◽  
Primary Defect ◽  
Onset Diabetes ◽  
Pancreatic Beta Cell Function

Maturity-onset diabetes of the young (MODY) is a relatively rare subtype of type 2 diabetes characterized by an early age of onset and autosomal dominant inheritance. Unlike type 2 diabetes, which is often associated with insulin resistance, MODY is caused by a primary defect in pancreatic beta-cell function resulting in a decrease in insulin secretion. Obesity is not a feature of MODY. However, environmental stressors that increase the demand for insulin, such as illness or puberty, may unmask the genetically limited insulin secretory reserve of the undiagnosed MODY patient. Euglycemia is the primary goal of therapy, and diet is the cornerstone of glycemic control. Sulfonylureas and/or exogenous insulin may also be required depending on the degree of dysfunction of the beta cells.

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