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3 "Protein malnutrition"
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Pancreatic beta-cell Function and Development in Male Offspring of Protein-Malnourished Rats.
Hyeong Kyu Park, Cheng Ji Jin, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2002;26(1):21-30.   Published online February 1, 2002
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BACKGROUND
Nutritional deprivation of the fetus and infant may be associated with susceptibility to impaired glucose tolerance or type 2 diabetes in adult life. This association has been interpreted as a long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues that regulate glucose metabolism. This study aimed to investigate the effect of protein malnutrition in a fetus and early life on the pancreatic beta-cell function and development. METHODS: Sprague-Dawley rats were fed a low-protein (8% casein) diet during pregnancy and lactation. Their male offspring were weaned onto either a control (18% casein) diet (recuperated group, R) or a low-protein diet (low-protein group, LP). The offspring of the rats fed control diet were weaned onto control diet (control group, C). Glucose tolerance tests and morphometry of the pancreas were performed to evaluate the pancreatic beta-cell function and development at the 25th week of age. RESULTS: Offspring of the protein-malnourished rats had a significantly lower body weights than the controls. The R and LP showed no major impairment in glucose tolerance, but the plasma insulin concentrations in the R (0.24+/-.03 nmol/L) and LP (0.28+/-.02 nmol/L) groups were lower at 20 min during IVGTT than the C (0.43+/-.05 nmol/L) groups. The areas under the curve for insulin (AUC insulin) during IVGTT were significantly lower in R and LP (0.39+/-.03 nmol/L/min, 0.43+/-.02 nmol/L/min) groups than the C (0.54+/-.03 nmol/L/min) group. In particular, the rats with fetal protein malnutrition showed severe impairment in late-phase insulin secretion to a glucose load. Both the pancreas weight and the proportion of the pancreas weight to the body weight were significantly lower in the R and LP groups than the C group. The proportion of beta-cells to pancreatic cells was lower in the LP (0.91+/-.14%) group than the C (2.19+/-.23%) and R (1.79+/-.25%) group. The relative beta-cell mass was significantly lower in the LP (by 62%) group that the C group. CONCLUSION: Rats with fetal protein malnutrition showed persistently impaired pancreatic beta-cell development and reduced insulin secretion capacity. These findings suggest that in utero protein malnutrition can contribute to the development of type 2 diabetes in adult life along with other deleterious environmental or genetic conditions.
Oxidative Stress and Antioxidative Defense System in Offspring of Protein-Malnourished Rats.
Eun Young Cho, Hyeong Kyu Park, Hyeon Jeong Jeon, Suk Kyeong Kim, Kyong Soo Park, Chong Ho Lee, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2001;25(3):190-199.   Published online June 1, 2001
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BACKGROUND
Free radical-mediated oxidative damage has been implicated in a variety of pathological processes such as diabetes mellitus, aging and atherosclerosis. The susceptibility of a given organism to oxidative damage is influenced by the overall balance between the degree of oxidative stress and antioxidative capabilities. Nutrition plays an important role in determining the cellular antioxidative defense mechanism. Thus, the aim of this study is to investigate the effects of fetal protein malnutrition on oxidative stress and antioxidative capabilities. METHOD: Rats were fed a low-protein (8% casein) diet throughout pregnancy and lactation. Male offspring were weaned onto either a control (18% casein) diet (group 2) or a low-protein diet (group 3). Offspring from rats fed a control diet were weaned onto a control diet (group 1). The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and the concentration of thiobarbituric acid- reactive substances (TBARS) were determined at 10 and 15 wk in liver and skeletal muscle from offspring. RESULTS: SOD activities of liver in group 3 were significantly lower than those in group 1 at 10 wk (4.14+/-0.65 U/mg protein, 9.09+/-0.85 U/mg protein) and 15 wk (4.18+/-0.58 U/mg protein, 7.63+/-0.74 U/mg protein), respectively. But SOD activities of skeletal muscle were not different between groups. Whilst GPx activities of liver were not different at 10 wk, GPx activities in group 2 (1.80+/-0.16 U/mg protein) were significant higher than those in group 1 (1.24+/-0.15 U/mg protein) at 15 wk. GPx activities of skeletal muscle were not different between groups. The TBARS concentrations in liver or skeletal muscle were not different between groups at 10 and 15 wk. There was a significant negative correlation between SOD activities and TBARS concentrations in liver (r=-0.359). CONCLUSION: In offspring of rats fed a low-protein diet throughout pregnancy and lactation, the antioxidant enzyme activities were significantly decreased, compared with offspring of rats fed a control diet. These alterations were not fully restored in low-protein offspring even when weaned onto a control diet. These results suggest that fetal protein malnutrition impair the antioxidative defense system.
The Combined Effects of Protein Malnutrition and Chronic Alcohol lntake on lnsulin Secretion and Sensitivity in Growing Rats.
Bong Soo Cha, Chul Woo Ahn, Hae II Lee, Yong Seok Yoon, Jae Kyeung Sung, Young Duk Song, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 2000;24(1):19-36.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
This investigation was performed to examine the combined effects of protein malnutrition and chronic moderate amount of alcohol intake on insulin secretory capacity and sensitivity in growing rats. METHODS: Weanling 4-week-old male Sprague-Dawley rats were fed low protein [5%, (wt/wt)] or control (C, 20%) diet from 4 to 12 weeks and alcohol (5g/kg/d) or saline gavage from 8 to 12 weeks. All rats were divided into the 4 groups according to different diet protocols: group 1 (protein-deficient alcohol rats), group II (protein-deficient saline rats), group III (protein-sufficient alcohol rats), and group IV (protein-sufficient saline or control rats), At the age of 12 weeks, we determined the insulin secretory capacity and sensitivity in the 4 different diet groups. RESULTS: The results are summarized as following: 1. Normal weight gain was nearly completely arrested in protein-deficient rats compared to control rats. In protein-sufficient rats, chronic alcohol intake decreased body weight gain. Pancreatic weight adjusted with body weight was not different among the 4 groups, but epididymal fat weight adjusted with body weight was decreased in group II compared to group IV. 2. Intraperitoneal glucose tolerance was improved in group I compared to the other groups. Insulin responses to glucose challenge were markedly decreased in group II compared to group IV, but not in group l. 3. Glucose disposal rate during euglycemic clamp test was diminished in group II compared to qroup IV, but there were no differences between group I and group I 3. Glycogen synthase activities of skeletal muscle after 2 hour hyperinsulinemic state were not different among the 4 groups. 4. There were no differences of reserved insulin content of whole pancreas adjusted with pancreas weight among the 4 groups. 5. In light microscopic findings of pancreatic islets, sizes of islets, islet cells and nuclei were decreased in protein-deficlent rats compared to control rats. However, the sizes of islet cells and nuclei were further decreased in group II compared to group l. CONCLUSION: These results suggest that impaired insulin secretion and decreased insulin sensitivity due to protein malnutrition can be restored by chronic, moderate amount of alcohol intake, but these beneficial effects may not be appeared in protein-sufficient state. Therefore, the chronic alcohol intake differently influences glucose metabolism according to individual nutritional status, and further studies for the effects of alcohol intake in lean diabetic patients are required to extrapolate these resuits in human.

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