Mechanisms by which poor early growth programs type-2 diabetes, obesity and the metabolic syndrome

2006 ◽  
Vol 88 (3) ◽  
pp. 234-243 ◽  
Author(s):  
D.S. Fernandez-Twinn ◽  
S.E. Ozanne
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Early Growth ◽  
The Metabolic Syndrome

Pre- and early postnatal nongenetic determinants of type 2 diabetes

2002 ◽  
Vol 4 (24) ◽  
pp. 1-14 ◽  
Author(s):  
Susan E. Ozanne ◽  
C. Nick Hales
Keyword(s):  
Gene Expression ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Hormone Receptors ◽  
Early Growth ◽  
Growth Restriction ◽  
Future Research ◽  
Thrifty Phenotype ◽  
The Metabolic Syndrome

Epidemiological studies have revealed strong and internationally reproducible links between early growth restriction and subsequent risk of developing type 2 diabetes and the metabolic syndrome (glucose intolerance, hypertension and hypertriglyceridaemia). This effect can exist independently of genetic factors. There is also direct evidence that poor maternal nutrition and maternal smoking cause both a reduction in birthweight and subsequent loss of glucose tolerance. High rates of growth in childhood may add to these effects. The ‘thrifty phenotype’ hypothesis attempts to explain these associations in terms of an altered programming of growth and metabolism that aids survival both pre- and postnatally. Type 2 diabetes is envisaged as a consequence of a clash of this programming with adult obesity. Tests of this hypothesis in animal models have shown that both the metabolic syndrome and type 2 diabetes can result from early growth restriction in rats consequent upon rat dams being fed a reduced protein, isocaloric diet (in which the protein is replaced by an equal quantity of nonprotein energy). A variety of other models of early growth restriction in rats lead to a similar phenotype. Several structural and gene expression changes have been shown in many tissues, including pancreas, liver, kidney, muscle and adipose tissue. Changes in gene expression include those concerned with hormone receptors, signalling and glycolytic enzymes. Many important questions remain for future research.

scholarly journals The Metabolic Syndrome in Overweight Hispanic Youth and the Role of Insulin Sensitivity

2004 ◽  
Vol 89 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Martha L. Cruz ◽  
Marc J. Weigensberg ◽  
Terry T.-K. Huang ◽  
Geoff Ball ◽  
Gabriel Q. Shaibi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Insulin Sensitivity ◽  
Family History ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Hdl Cholesterol ◽  
Hispanic Youth ◽  
The Metabolic Syndrome

The prevalence of the metabolic syndrome is highest among Hispanic adults. However, studies exploring the metabolic syndrome in overweight Hispanic youth are lacking. Subjects were 126 overweight children (8–13 yr of age) with a family history for type 2 diabetes. The metabolic syndrome was defined as having at least three of the following: abdominal obesity, low high-density lipoprotein (HDL) cholesterol, hypertriglyceridemia, hypertension, and/or impaired glucose tolerance. Insulin sensitivity was determined by the frequently sampled iv glucose tolerance test and minimal modeling. The prevalence of abdominal obesity, low HDL cholesterol, hypertriglyceridemia, systolic and diastolic hypertension, and impaired glucose tolerance was 62, 67, 26, 22, 4, and 27%, respectively. The presence of zero, one, two, or three or more features of the metabolic syndrome was 9, 22, 38, and 30%, respectively. After controlling for body composition, insulin sensitivity was positively related to HDL cholesterol (P < 0.01) and negatively related to triglycerides (P < 0.001) and systolic (P < 0.01) and diastolic blood pressure (P < 0.05). Insulin sensitivity significantly decreased (P < 0.001) as the number of features of the metabolic syndrome increased. In conclusion, overweight Hispanic youth with a family history for type 2 diabetes are at increased risk for cardiovascular disease and type 2 diabetes, and this appears to be due to decreased insulin sensitivity. Improving insulin resistance may be crucial for the prevention of chronic disease in this at-risk population.

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