- The Clinical Characteristics of Anemia in Type 2 Diabetic Patients Without Overt Nephropathy.
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Eun Young Ko, Se In Kim, Yong Bum Jang, Kyoung Hun Min, Sung Hun Kim, Kyu Sun Lee, So Ri Kim, Eun Kyoung Choi, Ji Hyun Park, Tae Sun Park, Hong Sun Paek
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Korean Diabetes J. 2004;28(5):425-431. Published online October 1, 2004
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Abstract
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- BACKGROUND
It is well known that anemia occurs early in diabetic patients before they reach to end stage renal failure. This anemia is considered to be due to the reduced endogenous erythropoietin synthesis, tubulointerstitial damage, autonomic dysfunction, and to the use of angiotensin-converting- enzyme inhibitors. Because anemia has a significant impact on the quality of life for diabetic patients, we examined the clinical characteristics of anemia in those diabetic patients who did not have overt nephropathy. METHODS: We retrospectively reviewed the medical records of 200 type 2 diabetic patients with anemia who had been followed up from 1998 to 2002 by Chonbuk University Medical School Hospital. We measured the total cholesterol, triglycerides, high density lipoprotein, low density lipoprotein, and the presence of complications (retinopathy or neuropathy) for about 90 diabetic patients who were under the age of 65, they were without other underlying disease and they had a hemoglobin concentration 110g/L, GFR 1.0 mL/s. We excluded the causes of anemia as being from malignancy, liver disease, coexisting iron deficiency, chronic inflammatory disease and chronic infection. RESULTS: The clinical characteristics of the patients are as follows; the mean age was 59.6 +/- 8.4 years, the mean HbA1C was 9.4 +/- 2.3%, and the mean Hb concentration was 96 +/- 12 g/L. Our results showed that an inverse relation existeds between Hb concentration and total cholesterol (p<0.04), LDL cholesterol (p<0.05), age (p<0.02), and the duration of diabetes (p<0.01).Our results also showed that a linear relation existed between the Hb concentration, HDL cholesterol (p<0.02), and the GFR (p<0.01). CONCLUSION: Diabrtic patients with anemia are in need of intensive management for the lipid and GFR that causes thair anemia.
- Serum Plasema Leptin Levels, Abdominal Obesity, and Insulin Resistance in Type 2 Diabetic Patients.
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Dae Won Jun, Sung Hun Kim, Jae Hyung Lee, Woong Hwan Choi, Yong Soo Park, Tae Hwa Kim
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Korean Diabetes J. 2000;24(2):216-224. Published online January 1, 2001
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Abstract
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- BACKGROUND
There is growing evidence for a adipoinsular axis, between adipose tissue and pancreatic beta cells via the hormones leptin and insulin, in mice models, Insulin is adipogenic and increases the production of leptin by adipose tissue, Leptin feeds back to reduce both insulin secretion and insulin gene expression. But human obesity is a complex disorder, with many factors playing a parts; the pathophysiology of leptin is not as simple as it seems to be in mice models of obesity. We therefore explored the dysregulation between leptin and insulin concentration in human model. METHOD: Using radioimmunoassay, we measured serum leptin concentrations in Type 2 diabetic patients (male 26, male 52). Using body composition, we measured total and regional adiposity. The data were analyzed using t-tast to test difference in serum leptin concentration, and other factors were evaluated by partial correlation analysis. RESULT: Serum leptin concentrations in both sex was strongly and positively correlated with total adiposity (r=0.588, p<0.001), Serum leptin concentration was correlated with serum insulin concentration (r=0.41, p=0.002) even after adjusting for adiposity in both sex (r=0.32, p=0.021). Serum leptin concentration was more highly correlated with abdominal adiposity than peripheral adiposity(r=0.693 vs r=0,628). Leptin concentration were higher in women than men, even at the same adiposity, However, no independent association was seen between leptin and hypertension as well as total cholesterol. CONCLUSION: Serum leptin concentration was correlated with serum insulin concentration even after adjusting for adiposity in both sex, In human, such a putative loss of leptin reception by beta cell could result in dysregulation of the adipoinsular axls and a corresponding failure to suppress insulin secretion, resulting in chronic hyperinsutinemia.
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