Curcuminoids Target Decreasing Serum Adipocyte-fatty Acid Binding Protein Levels in Their Glucose-lowering Effect in Patients with Type 2 Diabetes / 生物医学与环境科学（英文）

Whether supplementation of curcuminoids decreases serum adipocyte-fatty acid binding protein (A-FABP) level and whether this decrease benefits glucose control is unclear. One-hundred participants (n=50 administered curcuminoids, n=50 administered placebo) from our previous report on the effect of curcuminoids on type 2 diabetes in a 3-month intervention were assessed for levels of serum A-FABP, oxidative stress, and inflammatory biomarkers. Curcuminoids supplementation led to significant decreases in serum A-FABP, C-reactive protein (CRP), tumor necrosis factor-α, and interleukin-6 levels. Curcuminoids supplementation also significantly increased serum superoxide dismutase (SOD) activity. The change in serum A-FABP levels showed positive correlations with changes in levels of glucose, free fatty acids (FFAs), and CRP in subjects supplemented with curcuminoids. Further stepwise regression analysis showed that A-FABP was an independent predictor for levels of FFAs, SOD, and CRP. These results suggest that curcuminoids may exert anti-diabetic effects, at least in part, by reductions in serum A-FABP level. A-FABP reduction is associated with improved metabolic parameters in human type 2 diabetes.

Effects of beta glucan in highland barley on blood glucose and serum lipid in high fat-induced C57 mouse / 中华预防医学杂志

<p><b>OBJECTIVE</b>Study the effects of β-glucan in highland barley on blood glucose and serum lipid in high fat diet induced C57 mouse.</p><p><b>METHODS</b>Using table of random number, 40 male C57BL/6 mice were randomly divided into 4 groups (10 mice in each group) by weight: high dosage group (4% β-glucan and high fat diet), low dosage group (2% β-glucan and high fat diet), high fat diet group and normal control group. Food-intake and body weight of C57 mouse were observed. Glucose tolerance tests and examinations of fasting blood glucose were performed at the end of 11 weeks of intervention. Mice were sacrificed after 12 wk of treatment, and serum specimens were obtained to test relevant biochemical indicators.</p><p><b>RESULTS</b>After 12 weeks raise, among high dosage group, low dosage group, high fat diet group and normal control group, the weight was (32.8 ± 1.5), (40.4 ± 1.9), (40.7 ± 2.1) and (33.5 ± 1.3) g, respectively (F = 55.26, P < 0.05); average food intake was (3.48 ± 0.56), (3.69 ± 0.76), (3.66 ± 0.81) and (3.54 ± 0.61) g/d respectively (F = 0.26, P > 0.05); fasting blood-glucose was (5.29 ± 1.59), (6.13 ± 1.75), (7.63 ± 1.09) and (4.24 ± 0.98) mmol/L respectively (F = 9.54, P < 0.01); serum insulin level was (1.97 ± 0.10), (2.44 ± 0.24), (3.02 ± 0.36) and (1.48 ± 0.28) ng/ml respectively (F = 47.58, P < 0.01); the area under blood glucose concentration curve was (25.81 ± 1.44), (30.42 ± 2.01), (35.17 ± 1.20) and (21.03 ± 1.24) mmol×L(-1)×h(-1), respectively (F = 64.98, P < 0.05); insulin resistance index was (9.84 ± 3.78), (13.69 ± 4.48), (21.54 ± 3.27) and (5.81 ± 1.59) respectively (F = 30.18, P < 0.01); serum total cholesterol (TC) level was (4.05 ± 0.88), (4.30 ± 0.48), (4.73 ± 0.66) and (3.37 ± 0.40) mmol/L respectively (F = 6.70, P < 0.01); serum triglyceride (TG) level was (0.90 ± 0.09), (0.98 ± 0.09), (1.05 ± 0.06) and (0.76 ± 0.26) mmol/L respectively (F = 6.75, P < 0.01); serum high-density lipoprotein cholesterol (HDL-C) level was (2.91 ± 0.59), (3.34 ± 0.46), (4.89 ± 0.42) and (3.24 ± 0.37) mmol/L respectively (F = 31.73, P < 0.01); serum low-density lipoprotein cholesterol (LDL-C) level was (0.25 ± 0.15), (0.42 ± 0.19), (0.72 ± 0.12) and (0.32 ± 0.11) mmol/L, respectively (F = 17.27, P < 0.01); free fatty acids (FFA) level was (1.06 ± 0.03), (1.05 ± 0.05), (1.18 ± 0.32) and (1.04 ± 0.02) mmol/L, respectively (F = 1.36, P > 0.05); HDL-C/LDL-C was (13.77 ± 5.51), (9.11 ± 3.53), (7.04 ± 1.65) and (11.21 ± 3.31), respectively (F = 5.24, P < 0.01).</p><p><b>CONCLUSION</b>The β-glucan in highland barley reduced the serum glucose and serum lipid, as well as insulin resistance and the risk of arterial sclerosis in high-fat induced C57 mouse.</p>

Curcumin, a potential inhibitor of up-regulation of TNF-alpha and IL-6 induced by palmitate in 3T3-L1 adipocytes through NF-kappaB and JNK pathway / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the attenuating effect of curcumin, an anti-inflammatory compound derived from dietary spice turmeric (Curcuma longa) on the pro-inflammatory insulin-resistant state in 3T3-L1 adipocytes.</p><p><b>METHODS</b>Glucose uptake rate was determined with the [3H] 2-deoxyglucose uptake method. Expressions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by quantitative RT-PCR analysis and ELISA. Nuclear transcription factor kappaB p65 (NF-kappa p65) and mitogen-activated protein kinase (MAPKs) were detected by Western blot assay.</p><p><b>RESULTS</b>The basal glucose uptake was not altered, and curcumin increased the insulin-stimulated glucose uptake in 3T3-L1 cells. Curcumin suppressed the transcription and secretion of TNF-alpha and IL-6 induced by palmitate in a concentration-dependent manner. Palmitate induced nuclear translocation of NF-kappaB. The activities of Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase1/2 (ERK1/2) and p38MAPK decreased in the presence of curcumin. Moreover, pretreatment with SP600125 (inhibitor of JNK) instead of PD98059 or SB203580 (inhibitor of ERK1/2 or p38MAPK, respectively) decreased the up-regulation of TNF-alpha induced by palmitate.</p><p><b>CONCLUSION</b>Curcumin reverses palmitate-induced insulin resistance state in 3T3-L1 adipocytes through the NF-kappaB and JNK pathway.</p>

Effects of maternal high protein diet on uncoupling protein and carnitine palmityl transferase 1 in offspring of rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of maternal nutritional manipulation on fetal mRNA abundance of uncoupling protein UCP2, UCP3 and carnitine palmityl transferase 1 (CPT1), and find out an optimal maternal diet and targets for pharmacological prevention and treatment of obesity.</p><p><b>METHODS</b>Wistar pregnant rats were assigned to two groups which received a standard diet (SD) and a high protein diet (HPD) during pregnancy, respectively. After delivery, the male offspring were assigned to control group (CON) and high protein group (HP) according to their maternal diet, which were suckled by dams that received SD during pregnancy. Offspring were fed with SD from weaning (week 3) to week 8. Then CON were allocated to two groups: CON (SD during the whole experiment); HFCON (high fat control). HFCON and HP group rats were fed with high-fat diet (HFD) for 6 wk to induce obesity. At 0, 3, 8 and 14 wk of age, blood and tissue were collected for analyzing blood fat and abundance of UCP2, 3 and CPT1 mRNA.</p><p><b>RESULTS</b>In HP body weight and TG were decreased after weaning (F = 4.589, P = 0.039; F = 27.001, P = 0.000) and HFD (F = 16.076, P = 0.00; F = 71.518, P = 0.000). Obesity rates were significantly decreased in HP after HFD (chi2 = 8.076, P = 0.004). The abundance of UCP3 and CPT1 mRNA was persistently higher in HP than in CON or HFCON, and the abundance of UCP2 mRNA was also persistently higher than in CON or HFCON after weaning. Moreover the abundance of CPT1 mRNA was significantly increased after weaning and HFD compared with that after SD, the abundance of UCP2, UCP3 mRNA was also increased after HFD compared with that after SD.</p><p><b>CONCLUSIONS</b>Increasing protein intake during pregnancy might prevent offspring from HFD-induced obesity in adult, moreover might increase offspring the expression of UCP2, UCP3 and CPT1 mRNA. UCP2, UCP3 and CPT1 might participate in prevention and treatment of obesity by mediating fatty acid oxidation.</p>

Effects of conjugated linoleic acid on expression of GLUT4 protein in skeletal muscle of insulin resistant rat / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effects of conjugated linoleic acid (CLA) on expression of glucose transporter 4 (GLUT4) protein in skeletal muscle of insulin resistant rat, and explore the mechanism of resisting diabetes by CLA.</p><p><b>METHODS</b>Male Wistar rats were randomly separated into control group, high-fat group and high fat plus CLA group (0.75 g%, 1.50 g%, 3.00 g% by deit weight), and the effects of CLA on blood glucose and insulin levels of insulin resistant rat were observed , by using Western blot technique to measure the expression level of GLUT4 protein in skeletal muscle of insulin resistant rat.</p><p><b>RESULTS</b>The serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) microU/ml, and (5.09 +/- 0.66) mmol/L, the supplement of CLA might decrease the hyperinsulinemia and hyperglycemia, and in CLA groups (0.75 g%, 1.50 g%, 3.00 g% by deit weight) the serum insulin was (6.99 +/- 1.77) microU/ml, (7.36 +/- 1.48) microU/ml and (7.85 +/- 1.60) microU/ml (P < 0.05), and the glucose levels were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L (P < 0.05), (4.06 +/- 0.63) mmol/L (P < 0.05) respectively. The expression of GLUT4 protein in skeletal muscle of rat fed with high fat diet were decreased as compared with those fed with basic deit, and CLA might increase the expression of GLUT4 protein in skeletal muscle fed with high fat diet.</p><p><b>CONCLUSIONS</b>CLA improve the insulin resistance of obese rat, possibly acting through increasing the expression of GLUT4 protein in skeletal muscle of rat fed with high fat diet.</p>

The study on mechanism of appetite regulation in diet-induced obesity resistant rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore the cause of decreasing intake food of diet-induced obesity resistant (DIO-R) rats.</p><p><b>METHODS</b>Fifty male Sprague-dawley (SD) rats were randomly divided into control group and high-fat group and they were fed with basic diet and high-fat diet respectively for 13 weeks. DIO-R and diet-induced obesity (DIO) rats were selected according to their body weight and the quantity of energy intake, then observing the changes of the total food intake, the level of serum leptin and plasma NPY were determined by radioimmunoassay and the contents of the melanocortin receptor-4 (MCR-4) in brain were determined by Western Blot.</p><p><b>RESULTS</b>The total food intake of DIO-R rats was (1 679.1 +/- 146.8) g. The total food intake of DIO rats was (1 818.4 +/- 148.9) g. The total food intake of DIO-R rats was lower than that of DIO rats (P < 0.05). The level of plasma NPY of DIO-R rats was (795.24 +/- 83.59) ng/L. The level of plasma NPY of DIO rats was (1 007.14 +/- 172.83) ng/L. The level of plasma NPY of DIO-R rats was lower than that of the DIO rats (P < 0.05). The levels of serum leptin of basic, DIO-R and DIO rats was (4.80 +/- 0.75) microg/L, (9.17 +/- 1.19) microg/L and (9.32 +/- 1.04) microg/L. The level of serum leptin of rats in high-fat diet group was increased as compared with the rats in basic diet group, but there was no significant difference between DIO-R and DIO rats (P > 0.05). The levels of brain MCR-4 of basic, DIO-R and DIO rats were (342 +/- 31) mm2, (455 +/- 33) mm2, (355 +/- 30) mm2. High fat diets increased the content of brain MCR-4 in DIO-R rats.</p><p><b>CONCLUSION</b>DIO-R rats decreased appetite by increasing expression of ob gene to reduce activity of NPY pathway and activate the MCR-4 pathway, and thus inhibit the increase body of weight.</p>

Gene expression of resistin and the effect of conjugated linoleic acid on its expression of obese rat fed with high fat diet / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the gene expression of the resistin and the effects of conjugated linoleic acid on its expression in white adipose tissue of obese rats fed with high fat diet during the formation of insulin resistance.</p><p><b>METHODS</b>Male Wistar rats were randomly separated in control group, high-fat group and high fat + conjugated linoleic acid (CLA) group (0.75 g, 1.50 g, 3.00 g per 100 g diet weight), using reverse transcription polymerase chain reaction (RT-PCR) technique to measure the expression level of resistin and peroxisome proliferator-activated receptor-gamma (PPARgamma) mRNA expression.</p><p><b>RESULTS</b>the serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) mIU/L, (5.09 +/- 0.66) mmol/L, and supplement of CLA might decrease hyperinsulinemia and hyperglycemia, in CLA group (0.75 g, 1.50 g, 3.00 g per 100 g diet weight) the serum insulin levels were (6.99 +/- 1.77) mIU/L, (7.36 +/- 1.48) mIU/L, (7.85 +/- 1.60) mIU/L, and glucose levels were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L, (4.06 +/- 0.63) mmol/L. The expression of resistin in adipose tissue of obese rat fed with high fat diet was increased as compared with those fed with basic diet. CLA might increase the expression of resistin and PPARgamma in adipose tissue of obese rat.</p><p><b>CONCLUSION</b>The expression of resistin mRNA of obese rat fed with high fat diet was higher than those fed with basic diet, and CLA might improve the insulin resistance in obese rats and possibly upregulate the expression of resistin through activing PPARgamma.</p>

Effect of conjugated linoleic acid on gene expression of adiponectin of obese rat fed with high fat diet / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effect of conjugated linoleic acid (CLA) on expression of adiponectin in white adipose tissue of obese rats.</p><p><b>METHODS</b>Male Wistar rats were randomly divided into control group, high-fat group and high fat + CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight), we observed the effect of CLA on serum insulin and glucose levels of obese rats, and the reverse transcription polymerase chain reaction (RT-PCR) technique was used to measure the expression level of adiponectin and peroxisome proliferator-activated receptor-gamma (PPARgamma) mRNA.</p><p><b>RESULTS</b>The serum insulin and glucose levels of obese rats were (11.11 +/- 2.73) microIU/ml, (5.09 +/- 0.66) mmol/L. The supplement of CLA decreased the hyperinsulinemia and hyperglycemia, the serum insulin in CLA group (0.75 g, 1.50 g, 3.00 g per hundred gram diet weight) were (6.99 +/- 1.77) microIU/ml, (7.36 +/- 1.48) microIU/ml, (7.85 +/- 1.60) microIU/ml (P < 0.05), and glucose were (4.28 +/- 0.72) mmol/L, (4.18 +/- 0.55) mmol/L (P < 0.05), (4.06 +/- 0.63) mmol/L (P < 0.05), CLA can increase the expression of adiponectin and PPARgamma in adipose tissue of obese rat.</p><p><b>CONCLUSION</b>The CLA might improve the insulin resistance of the obese rat and increase the expression of adiponectin mRNA, which might possibly act through activating PPARgamma.</p>

Role of leptin in development of peripubertal boys / 中华预防医学杂志

<p><b>OBJECTIVES</b>To study the role of leptin in the development boys during their puberty and its relationship with insulin (INS), growth hormone (GH), estradiol (E2) and testosterone (T).</p><p><b>METHODS</b>One hundred and fifty boys with simple obese aged 7 to 17 years, 150 normal healthy boys and 150 boys with malnutrition matched for age (+/- 3 months) and height (+/- 2 cm) were selected. Serum levels of leptin, INS, GH, E2 and T were measured for them.</p><p><b>RESULTS</b>Serum level of leptin in obese group was significantly higher than that in normal group, and that in normal group was significantly higher than that in malnourished group. In the all three groups, serum level of leptin increased with age first until peak value, then began to decrease, with peak value of 6.96 microg/L at ages of 10-11 y in obese group, 10.25 microg/L at ages of 11-12 y in normal group and 5.08 microg/L at ages of 11-12 y in malnourished group. Serum level of leptin increased steadily from Tanner stages G1 to G2, then began to decrease steadily in G2 to G4. Serum level of leptin increased again in stage G5. Serum level of INS in boys increased steadily with age from 7 to 17 years old. Serum levels of GH, T and E2 in boys began to increase since 10-11 years old. Serum level of leptin positively correlated with serum level of INS and negatively correlated with serum levels of GH and T, but not correlated with serum level of E2.</p><p><b>CONCLUSIONS</b>Leptin may promote pubertal development of boys, but not the determinant factor in triggering and maintaining their pubertal development. Re-increase in level of leptin during stage G5 could inhibit secretion of GH, and signalize the end of puberty in boys.</p>

A study on the factors influencing insulin resistance in children and adolescents / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore the factors influencing insulin resistance in children with different nutritional status during pubertal development.</p><p><b>METHODS</b>Three hundred children with simple obese aged 7 to 17 years, and 300 normal healthy children and 300 children with malnutrition, matched for age (+/- 3 months) and height (+/- 2 cm), were selected. Fasting serum levels of leptin, insulin, glucose, total cholesterol (TC), triglycerides (TG), low density lipoprotein-cholesterol (LDL-C) and high density lipoprotein-cholesterol (HDL-C) were measured for them.</p><p><b>RESULTS</b>Levels of fasting serum insulin in obese children, except for boys at Tanner stage I and girls at Tanner stage II, were higher than those in normal and malnutrition children (P < 0.01). Average serum level of leptin in obese boys and girls at varied Tanner stages was higher than that in normal children, and higher in normal children than that in children with malnutrition (P<0.01). Serum level of TG in obese children [(1.53 +/- 0.13) mmol/L] was higher than that in normal ones [(1.12 +/- 0.10) mmol/L] and in children with malnutrition [(1.03 +/- 0.09) mmol/L]. There was no significant difference in levels of fasting blood glucose and other blood lipids between the three groups of children. Insulin sensitivity decreased with pubertal development and its index reversely correlated with Tanner stage and serum level of leptin (r=-0.27 and -0.36, respectively, P<0.01).</p><p><b>CONCLUSION</b>Obesity (BMI), serum level of leptin and pubertal development were independent risk factors for insulin resistance in children aged 7 to 17 years.</p>

Expression of hormone-sensitive lipase mRNA in diet-induced obesity resistant rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>In order to explore the expression of hormone-sensitive lipase (HSL) mRNA in white adipose tissue of diet-induced obesity-resistant (DIO-R) rats.</p><p><b>METHODS</b>Fifty male Sprague-dawley (SD) rats were randomly divided into control group and high-fat group and they were fed with basic diet and high-fat diet respectively for 13 weeks. DIO-R and DIO rats were selected according to their body weight and the quantity of energy intake, then observing changing of the body fat content, the level of serum growth hormone was determined by radioimmunoassay and the level of the HSL mRNA in white adipose tissue was determined by RT-PCR.</p><p><b>RESULTS</b>The body fat content of DIO-R rats were lower than those of DIO rats (P < 0.05). The level of serum growth hormone of DIO-R rats were higher than those of DIO rats (P < 0.05). High fat diets increased the level of the HSL mRNA in DIO-R rats.</p><p><b>CONCLUSION</b>Increasing expression of HSL in white adipose tissue may play a part of role in resisting diet-induced obesity of rats.</p>

Expression of uncoupling protein-2 mRNA in diet-induced obesity-resistant rats / 中华预防医学杂志

<p><b>OBJECTIVE</b>To explore the expression of uncoupling protein-2 mRNA in brown adipose tissue, white adipose tissue and skeletal muscle of diet-induced obesity-resistant (DIO-R) rats.</p><p><b>METHODS</b>Fifty male Sprague-Dawley (SD) rats were randomly divided into a control group and a high-fat group and fed with basic diet and high-fat diet respectively for 13 weeks. DIO-R and DIO rats were selected according to their body weight. The change of body weight and the intake of total calorie were observed. Reverse transcription-polymerase chain reaction (RT-PCR) was used to measure the expression of UCP2 mRNA in rat.</p><p><b>RESULTS</b>Body weight and total calorie intake in DIO-R rats (425.1 +/- 27.1) g, (31,693 +/- 946) kJ were significantly lower than those in DIO rats (489.7 +/- 20.5) g, (34,363 +/- 1465) kJ. The peak area of UCP2 mRNA in white adipose tissue in DIO-R rats was 352 +/- 30 and in DIO rats was 101 +/- 12. The peak areas of UCP2 mRNA in skeletal muscle in DIO-R and DIO rats were 130 +/- 15 and 170 +/- 12, respectively. The peak areas of UCP2 mRNA in brown adipose tissue of DIO and DIO-R rats were 124 +/- 14 and 147 +/- 19, respectively.</p><p><b>CONCLUSION</b>The expression of UCP2 mRNA in white adipose tissue of DIO-R rats increased significantly. These results suggest that obesity-resistance was associated with a tissue-specific increase in UCP2 expression.</p>

Roles of leptin in the development during girls'puberty / 中华预防医学杂志

<p><b>OBJECTIVES</b>To study the roles of leptin in the development during puberty in girls and the its relationship with insulin (INS), growth hormone (GH), estradiol (E(2)) and testosterone (T).</p><p><b>METHODS</b>One hundred and fifty girls with simple obese aged 7 to 17 years, and 150 normal healthy girls and 150 girls with malnutrition matched for age (+/- 3 months) and height (+/- 2 cm) were selected. Serum levels of leptin, INS, GH, E(2) and T were measured for them.</p><p><b>RESULTS</b>Their serum level of leptin positively correlated with body mass index (BMI) and age. Serum level of leptin in girls increased steadily from Tanner stage B(1) to stage B(5). At Tanner stage B(2), serum level of leptin in the normal groups (7.72 microg/L) was not significantly different from that in those with malnutrition (7.36 microg/L), but significantly lower than that in the obese groups (12.85 microg/L). At other Tanner stages, there was significant difference in serum level of leptin among obese, normal and malnutrition groups. Serum level of leptin correlated negatively with serum GH and positively with serum INS, but not correlated with E(2) and T.</p><p><b>CONCLUSIONS</b>Leptin may play a role in triggering development during puberty in girls. Serum level of leptin at Tanner stage B(2) may be the threshold dose to trigger the onset of puberty in girls. Quickly increasing level of leptin at Tanner stage B(5) may inhibit the increase of GH, which ushered the end of puberty in girls.</p>