Objectives : The aim of this study was to investigate the effects of licorice supplementation on muscle injury, plasma cortisol, testosterone and insulin sensitivity after high intensity resistance exercise. Methods : The fourteen health college male students were voluntarily participated in this study and were randomly divided into 2 groups: Control group (CON, n=7), Licorice group (LR, n=7). LR group ingested 2 g/time of licorice extract (mixed with 100 ml of water) two times/day for 10 days while the CON group ingested 100 ml of water. All subjects performed a high intensity resistance exercise (half-squat, 8 RM at 80% one-repetition maximum, 5 sets, 1min rest). Blood samples were collect before (-7) and after (0) licorice supplementation, and then 1 day, 2 day and 3 day post exercise. After 10 day treatment, plasma creatine kinase, cortisol, testosterone, glucose, insulin were measured. To determine the insulin sensitivity, HOMA-IR was calculated. Results : Plasma creatine kinase activities were significantly elevated after exercise, but there was not different between two groups. The plasma cortisol and testosterone levels were not significantly different between two groups. Plasma glucose levels were increased at 1 day and 2 day after exercise in the LR comparing with CON group (P<0.05) but plasma insulin levels were significantly lower in comparison with CON. HOMA-IR were significantly lower in the LR than CON group at 0 day to 3 day (P<0.05). Conclusions : The results of the current study suggest that licorice supplementation for 10 days might not attenuate the high-intensity exercise-induce muscle injury but may enhance the whole-body insulin sensitivity.
There is substantial evidence that insulin sensitivity can be enhanced through appropriate dietary management . In this study, insulin sensitivity was evaluated using and insulin suppression test. Male Sprague-Dawley rats, were caused to be in a diabetic condition by the injection of streptozotocin, and divided into four groups. They were fed one of the following diets for 2 weeks : (group 1) a high-carbohydrate(CHO) low-fat low-fiber diet, (group 2) a high CHO low-fat and high-fiber diet, (group 3) a low-CHO high-fat and low-fiber diet, and (group 4) a low-CHO low-fat diet groups (as comparison between group 1 and group 2 shows). In the low-CHO high-fat diet groups, dietary fiber tended to decrease plasma glucose levels at the end of the experiment, but not significantly (as comparison between group 3 and group 4 shows). The average steady state plasma glucose level in rats on the group 3 diet was the highest among all four groups(p<0.05), indicating the poorest insulin sensitivity . However, high fiber increased insulin sensitivity in rats on the low-CHO high-fat diets(as shows by a comparison between group 3 and group 4). On the other hand , the high-CHO low-fat enhanced insulin sensitivity in rats on the low fiber diet(group 1 and group 3). The degree of enhancement of insulin sensitivity depends on the combination of CHO, fat , and fiber in the diet. In conclusion, this study demonstrates that a low-CHO high-fat low -fiber diet may be deleterious to diabetic rats. In view of insulin sensitivity enhancement , dietary fiber level is irrelevant, as long as the diet has a high-CHO and low-fat level.
To examine whether colostral growth factors are transferred to the general circulation, concentrations of plasma cortisol, insulin, prolactin, growth hormone, insulin-like growth factors(IGFs) -I and -II, IGF-binding proteins(IGFBPs) and total protein were measured in newborn calves fed colostrums, milk of milk replacer before and after feeding at 12 h intervals during the first two days after birth. Plasma protein concentrations increased with time after than in milk- or milk replacer-fed calves. The mean protein concentration was greater in colostrum-fed than in milk- or milk replacer-fed calves. Plasma cortisol levels transiently declined after each feeding regardless of the type of diet, while insulin levels tended to increase. Mean concentrations of these hormones did not differ between dietary groups, nor did they change with time after birth. Plasma concentrations of prolactin and growth hormone did not differ between dietary groups and also did not change with time after birth or after feeding. Concentrations of IGF-I and IGF-II transiently increased at the second feeding period, but these, as well as plasma IGFBP profiles, were not different between groups or before and after feeding. Results did not indicate significant transfer of colostral growth factors across the newborn ruminant small intestine.
The objective of this study was to examine the effect of plasma leptin and insulin concentrations on fat traits in Hanwoo. If a biological indicator such as plasma leptin and insulin was identified, it would be a useful biological marker that can be predicted marbling score in young animal. The relationship between plasma hormone (leptin and insulin) and fat traits (marbling score, back fat thickness and P8 fat thickness) was investigated. The experiment studies 100 Hanwoo that were randomly sampled from Hanwoo Experimental Station Herd. The concentration of plasma insulin was significantly associated with marbling score (P=0.02) but was not significantly with back fat thickness (P=0.07) and P8 fat thickness (P=0.09). Statistical model determinant that plasma insulin concentration account for phenotypes was moderate on marbling score (5%), back fat thickness (3%) and P8 fat thickness (9%). On the other hand, plasma leptin concentration was significantly associated with marbling score (P=0.03) and back fat thickness (P=0.02), but was not significant on P8 fat thickness (0.07). Statistical model determinant that plasma leptin concentration accounting for phenotypes was moderate effect on marbling score (3%) and back fat thickness (2%), but it has a slightly bigger effect on P8 fat thickness (7%). In conclusion, the plasma leptin and insulin seems to have an effect on fat traits (marbling score, backfat thickness and P8 fat thickness) in Hanwoo.
What makes glucose transport function sensitive to insulin in one cell type such as adipocyte, and insensitive in another such as liver cells is unresolved question at this time. Recently it is known that insulin stimulates glucose transport in adipocytes largely by redistributing transporter from the storage pool that is included in a low density microsomal fraction to plasma membrane. Therefore, insulin sensitivity may depend upon the relative distribution of gluscose transporters between the plasma membrane and in an intracellular storage compartment. In hepatocytes, the subcellular distribution of glucose transporter is less well documented. It is thus possible that the apparent insensitivity of the hepatocyte system could be either due to lack of the constitutively maintained, intracellular storage pool of glucose transporter or lack of insulin-mediated transporter translocation mechanism in this cell. In this study, I examined if any intracellular glucose transporter pool exists in hepatocytes and this pool is affected by insulin. The results obtained summarized as followings: 1) Distribution of subcellular fractions of hepatocyte showed that there are $24.9{\pm}1.3%$ of plasma membrane, $36.9{\pm}1.7%$ of nucleus-mitochondria enriched fraction, $23.5{\pm}1.2%$ of lysosomal fraction, $9.6{\pm}1.0%$ of high density microsomal fraction and $4.9{\pm}0.5%$ of low density microsomal fraction. 2) In adipocyte, there were $29.9{\pm}2.6%$ of plasma membrane, $19.4{\pm}1.9%$ of nucleus-mitochondria enriched fraction, $26.7{\pm}1.8%$ of high density microsomal fraction and $23.9{\pm}2.1%$ of low density microsomal fraction. 3) Surface labelling of sodium borohydride revealed that plasma membrane contaminated to lysosomal fraction by $26.8{\pm}2.8%$, high density microsomal fraction by $8.3{\pm}1.3%$ and low density microsomal fraction by $1.7{\pm}0.4%$ respectively. 4) Cytochalasin B bound to all of subcellular fractions with a Kd of $1.0{\times}10^{-6}M$. 5) Photolabelling of cytochalasin B to subcellular fractions occurred on 45 K dalton protein band, a putative glucose transporter and D-glucose inhibited the photolabelling. 6) Insulin didn't affect on the distribution of subcellular fractions and translocation of intracellular glucose transporters of hepatocytes. 7) HEGT reconstituted into hepatocytes was largely associated with plasma membrane and very little was found in low density microsomal fraction which equals to the native glucose transporter distribution. Insulin didn't affect on the distribution of exogeneous glucose transporter in hepatocytes. From the above results it is concluded that insulin insensitivity of hepatocyte may due to lack of intracellular storage pool of glucose transporter and thus intracellular storage pool of glucose transporter is an essential feature of the insulin action.
Kim, Youn-Young;Kang, Hyo-Joo;Ko, Sung-Kwon;Chung, Sung-Hyun
Archives of Pharmacal Research
/
v.25
no.6
/
pp.923-931
/
2002
Sopungsungi-won (SP) is a known for\mula for senile constipation and diabetes mellitus, based on traditional Korean medicine. The preventive effect of SP on the development of overt diabetes in Zucker diabetic fatty (ZDF) rats was evaluated. When administered orally through a diet for 8 weeks, diabetic conditions such as hyperglycemia, polydipsia and hypertriglyceridemia were all ameliorated in SP-treated rats. In parallel with the onset and progression of hyperglycemia in the ZDF control rats; there was a marked decline in plasma insulin concentrations from 26.1 $\mu$U/ml, at age 7 weeks, to 14.8 $\mu$U/ml at age 15 weeks. In the SP-treated rats, however, the plasma insulin concentrations did not decline, and SP at a dose of 5 g/kg significantly increased the insulin levels to 31.9 $\mu$U/ml. Early normalization of plasma insulin and a retained ability to subsequently increase plasma insulin were indicative of a pancreatic $\beta$ cell protective action by the SP for\mula. In addition, expressions of an insulin-responsive gene and corresponding protein, glucose transporter 4 (GLUT4), in skeletal \muscle, were also determined in SP- and rosiglitazone-treated ZDF rats. mRNA and protein levels of GLUT4 in SP-treated rats were upregulated in a dose dependent manner. Furthermore, when ZDF rats were treated with 2 g/kg of the SP for\mula, the activity of glucose-6-phosphatase was decreased by 49%, whereas the activity of glucokinase was increased by 196%, compared to the ZDF control rats. Taken together, these data provide evidence that the SP for\mula markedly lowered the plasma glucose levels, probably through an effect not only on improvement of insulin action, but through a combined sti\mulation of glycolysis and an inhibition of gluconeogenesis in the liver, and also suggest the validity of SP's clinical use in the treatment of type 2 diabetes mellitus following further toxicological investigation.
Kim Sohye;Hong Kyunghee;Jang Ki-Hyo;Kang Soon Ah;Choue Ryowon
Nutritional Sciences
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v.8
no.4
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pp.250-255
/
2005
The purpose of this study was to investigate the relationship among plasma leptin, lipid profiles, insulin levels, and percentage of body fat of 72 schoolchildren from Obese Clinic Center in Seoul. The subjects divided into two groups: 39 obesity children [obesity index greater than $20\%$] who did not have a discernable medical cause of their obesity and 33 children with a obesity index less than $20\%$. The mean age, height, and obesity index of the subjects were 10.4 years, 144.0 cm, and $21.3\%$, respectively. The mean glucose and insulin levels of the obese children were 80.5 mg/dl and $13.3\;{\mu}IU/mL$ and those of the non obese children were 82.0 mg/dl and $4.2\;{\mu}IU/mL$, respectively. Obese children had significantly (p<0.05) higher level of total cholesterol, triglyceride, VLDL-cholesterol, LDL-cholesterol, and insulin concentration than non-obese children. However obese children had a lower level of HDL-cholesterol than non-obese children. Plasma leptin level were also positively correlated with BMI (p<0.000l), body fat (p<0.0001), tricep skinfold thickness (p<0.0001), mid arm circumference (p<0.0001), and waist hip ratio (p<0.0001). Plasma leptin showed a significantly positive correlation with insulin (p<0.0001), total cholesterol (p<0.0001), LDL-cholesterol (p<0.0001), and triglyceride (p<0.0001) levels, however, it was negatively correlated with HDL-cholesterol (p<0.0001) levels. In conclusion, the concentration of leptin in the blood is significantly correlated with the amount of body fat, BMI, plasma insulin, and plasma lipid profiles.
The advantages of monounsaturated fatty acids (MUFAs) on insulin resistance and type 2 diabetes mellitus (T2DM) have been well established. However, the molecular mechanisms of the anti-diabetic action of MUFAs remain unclear. This study examined the anti-hyperglycemic effect and explored the molecular mechanisms involved in the actions of fish oil- rich in MUFAs that had been acquired from hybrid catfish (Pangasius larnaudii${\times}$Pangasianodon hypophthalmus) among experimental type 2 diabetic rats. Diabetic rats that were fed with fish oil (500 and 1,000 mg/kg BW) for 12 weeks significantly reduced the fasting plasma glucose levels without increasing the plasma insulin levels. The diminishing levels of plasma lipids and the muscle triglyceride accumulation as well as the plasma leptin levels were identified in T2DM rats, which had been administrated with fish oil. Notably, the plasma adiponectin levels increased among these rats. The fish oil supplementation also improved glucose tolerance, insulin sensitivity and pancreatic histological changes. Moreover, the supplementation of fish oil improved insulin signaling ($p-Akt^{Ser473}$ and p-PKC-${\zeta}/{\lambda}^{Thr410/403}$), $p-AMPK^{Thr172}$ and membrane GLUT4 protein expressions, whereas the protein expressions of pro-inflammatory cytokines (TNF-${\alpha}$ and nuclear NF-${\kappa}B$) as well as p-PKC-${\theta}^{Thr538}$ were down regulated in the skeletal muscle. These data indicate that the effects of fish oil-rich in MUFAs in these T2DM rats were partly due to the attenuation of insulin resistance and an improvement in the adipokine imbalance. The mechanisms of the anti-hyperglycemic effect are involved in the improvement of insulin signaling, AMPK activation, GLUT4 translocation and suppression of pro-inflammatory cytokine protein expressions.
Plasma concentrations of Vitamins E and A were measured in 15 non-insulin dependent Korean female subjects and 15 age-matched normal subjects using reversed-phase high-performance liquid chromatography. No differences were found in plasma Vitamin E concentrations between the 2 groups. Plasma Vitamin A concentrations were higher in subjects with non-insulin dependent diabetes melitus (NIDDM). The effects were evaluated of 4 weeks of daily supplementation of 400 mg Vitamin E on plasma levels of these two vitamins. In addition, the effects were observed for Vitamin E supplementation on oxidative stress and immune-related compound productions in non-insulin dependent diabetic patients and control subjects. After treatment with Vitamin E, plasma Vitamin E concentrations were significantly elevated in both groups. Basal plasma thiobarbituric acid reactive substances (TBABS) were identical, and a decreased level of TBARS caused by Vitamin E was observed only in the diabetic group (0.02739$\pm$0.0024 versus 0.01814$\pm$0.0008 nmols malondialdehyde equivalents/dl plasma ; p<0.05). The basal and after-treatment levels of immunoglobulins A, G, M were identical in control and diabetic groups, indicating that Vitamin E did not appear to alter gross humoral responses in this study. However, elevation of Complement 3 ($C_3$) was noticed due to Vitamin E supplementation, revealing a possible effect of vitamin E on one aspect of humoral immunity, Furthermore, an increase in prostaglandin E_2 ($PGE_2$) levels in diabetic patients was normalized by Vitamin E supplementation. This suggests indirectly that the depressed cell-mediated response due to elevated $PGE_2$ could be normalized. For the definitive antioxidant intake recommendations for prevention and treatment of adverse effects of non-insulin dependent diabetes, evidence from intervention trials like this study should be collected. The present data suggests that Vitamin E may oxen some protective effects against oxidative damage and might have beneficial effects of partial immune-stimulation.
Six 16 months old Holstein steers were offered ad libitum feed for 7 months, to determine the (1) relationships of backfat thickness (BFT) to plasma leptin, and insulin; and (2) associations of TDN intake/kg body weight (BW) to plasma leptin, BFT and insulin. Feed intake, body weight and BFT were measured on selected monthly ages from day 1 to 8, day 1 and 8, and day 8, respectively. Blood was sampled on day 8 and the plasma was analyzed for leptin, insulin, glucose, NEFA, total cholesterol and triglyceride. Body weight and BFT increased, while TDN intake per kg BW decreased from 16 to 23 months old. Plasma leptin increased and mimicked the level of insulin, resulting to significant correlation (r=0.54; p<0.002). TDN intake was negatively related to plasma leptin (r=0.49; p<0.004), insulin (r=0.41; p<0.02) and BFT at 12 to 13th rib (r=0.48; p<0.005). Backfat thickness at 12 to 13th rib was positively related to plasma leptin (r=0.45; p<0.01). Negative associations of TDN intake with plasma leptin and BFT during finishing period suggest long-term involvement of adipose tissues in the feed intake regulation of steers fed high concentrate diet.
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