Decreased obestatin in plasma in metabolically obese, normal-weight men with normal glucose tolerance

2008 ◽  
Vol 79 (1) ◽  
pp. e5-e6 ◽  
Author(s):  
Xin-Yuan Gao ◽  
Hong-Yu Kuang ◽  
Xiao-Min Liu ◽  
Xue-Yan Wang ◽  
Yan-Hui Pan ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Normal Weight ◽  
Normal Glucose ◽  
Metabolically Obese Normal Weight

scholarly journals Inflammatory mediators in morbidly obese subjects: associations with glucose abnormalities and changes after oral glucose

2009 ◽  
Vol 161 (3) ◽  
pp. 451-458 ◽  
Author(s):  
Dag Hofsø ◽  
Thor Ueland ◽  
Helle Hager ◽  
Trond Jenssen ◽  
Jens Bollerslev ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Inflammatory Mediators ◽  
Interleukin 1 ◽  
Tolerance Test ◽  
Normal Glucose Tolerance ◽  
Normal Weight ◽  
Morbidly Obese ◽  
Oral Glucose ◽  
Cross Sectional ◽  
Normal Glucose

ObjectiveTo explore inflammatory mediators in morbidly obese (MO) subjects with various categories of glucose tolerance and to study the changes in these mediators after an oral glucose load.DesignCross-sectional and experimental study.MethodsA total of 144 MO subjects were classified into three categories: normal glucose tolerance (NGT); pre-diabetes; and new onset diabetes mellitus (NODM) were included, as were 27 normal weight normoglycemic controls. Serum osteoprotegerin (OPG), visfatin, leptin, adiponectin, interleukin-1 receptor antagonist (IL-1Ra), and C-reactive protein (CRP) were analyzed during an oral glucose tolerance test (OGTT).ResultsFasting levels of leptin and IL-1Ra were consistently higher in obese persons (P<0.001 and P<0.05). MO subjects with NGT had higher CRP levels (P<0.001) and lower adiponectin levels (P<0.05) compared to controls. Yet when compared with MO subjects with NODM, those with NGT had lower CRP levels and higher adiponectin levels (both P<0.05). Baseline OPG and visfatin levels did not differ between the groups (P=0.326 and P=0.198). During OGTT, OPG levels decreased (P<0.001) and visfatin levels increased transiently (P=0.018). The response in OPG and visfatin did not differ between the groups (P=0.690 and P=0.170). There were minor changes in adiponectin and leptin levels.ConclusionsMorbid obesity and glucose intolerance were associated with lower adiponectin levels and higher CRP levels, thus supporting a relationship between obesity, glucose homeostasis, and inflammation. Oral glucose suppressed OPG levels and transiently enhanced visfatin levels independent of obesity and glucose tolerance status, indicating that glucose may be involved in the acute regulation of these proteins.

STUDIES IN CONGENITAL GENERALIZED LIPODYSTROPHY (SEIP-BERARDINELLI SYNDROME)

1973 ◽  
Vol 72 (3) ◽  
pp. 475-494 ◽  
Author(s):  
Svein Oseid
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Juvenile Form ◽  
Congenital Generalized Lipodystrophy ◽  
Glucose Levels ◽  
Normal Glucose ◽  
Glucose Tolerance Tests ◽  
The One ◽  
Adipose Organ

ABSTRACT Six cases of congenital generalized lipodystrophy have been studied at different ages from infancy to adolescence with regard to glucose tolerance, insulin secretion, and insulin sensitivity. During the first few years of life there is normal glucose tolerance. The fasting immuno-reactive insulin (IRI) levels are either slightly elevated or normal. The IRI response to glucose is exaggerated and prolonged, at least from the third year of life. Some degree of insulin resistance is already present in infancy. From the age of 8–10 years glucose tolerance decreases rapidly. The fasting IRI levels are usually grossly elevated, while fasting plasma glucose levels are only moderately elevated or normal. The IRI responses to oral and iv administered glucose, and to tolbutamide are exaggerated; the insulinogenic indices are high. Cortisone primed glucose tolerance tests become abnormal. Insulin resistance is marked, and increases with age. After cessation of growth at approximately 12 years of age, frank diabetes with fasting hyperglycaemia and diabetic glucose tolerance curves developed in the one patient followed beyond this age. Her fasting IRI was increased, but there was a poor IRI response to glucose stimulation, suggesting a partial exhaustion of the β-cells. Her initial IRI response to tolbutamide was still good, but not as brisk as in the younger patients. This type of diabetes is quite different from the juvenile form, and also from the diabetes of older age. It may be causally related to the lack of an adequate adipose organ necessary for the disposal of excesses of glucose, or possibly related to another anti-insulin mechanism.

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