早期低脂肠内营养对急性重症胰腺炎血清甘油三酯的影响

目的观察早期低脂肠内营养（EEN）治疗对急性胰腺炎（SAP）血清甘油三酯水平的影响。方法将34例SAP并发高脂血症患者随机分为实验组和对照组,给予内镜下置管早期肠内营养治疗,16例实验组患者给予低脂要素肠内营养,18例对照组患者给予标准营养液肠内营养治疗,观察治疗前后甘油三酯（TG）、白细胞（WBC）、C反应蛋白（CRP）、谷草转氨酶（AST）、血钙及血糖的变化。结果两组患者治疗前后甘油三酯水平均明显下降,但实验组甘油三酯水平下降更加显著,且白细胞（WBC）、C反应蛋白（CRP）、谷草转氨酶（AST）、血钙与对照组比较下降更加明显,治疗前后血糖下降显著,治疗后两组比较差异不显著,考虑与均采用胰岛素降糖治疗有关。结论低脂EEN能够有效降低SAP甘油三酯水平并降低炎症反应、改善病情。     

核糖体蛋白S6激酶1基因沉默对高脂喂养小鼠肝脏炎性因子和肝脏胰岛素抵抗的影响

目的研究核糖体蛋白S6激酶1（S6K1）基因沉默对肝脏炎性因子表达的影响,探讨S6K1在肝脏胰岛素抵抗中的作用机制。方法将48只体重12．6～14．8g的6周龄雄性C57BL／6J小鼠按随机数字表法分为4组：普食对照组[普通饲料（ND）＋含U6启动子空载体腺病毒组（pU6Ax组）,即ND＋pU6Ax组]、普食实验组[ND＋S6K1短发夹RNA（shRNA）重组基因腺病毒组,即ND＋S6KIAx组]、高脂对照组[高脂饲料（HFD）’pU6Ax组,即HFD＋pU6Ax组]、高脂实验组（HFD＋S6K1Ax组）,分别喂养16周。实验组和对照组尾静脉分别注射S6K1Ax、pU6Ax（均为普食实验组及对照组90ml,高脂实验组及对照组120ml,效价为2．0×10^10pfu／m1）。注射后第6天过夜饥饿后,4组各随机抽取6只行葡萄糖耐量实验,剩余的小鼠处死取肝脏,逆转录-聚合酶链反应（RT—PCR）检测肝脏炎性因子单核细胞趋化蛋白-1（MCP-1）、肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-6、IL-10mRNA的表达,Western blotting观察肝脏蛋白S6K1、S6K1苏氨酸389（S6K1-thr389）、胰岛素受体底物1（IRS1）丝氨酸1101（IRS1-ser1101）、IRS1丝氨酸636／639（IRS1-ser636／639）、蛋白激酶B丝氨酸473（Akt—ser473）、c—Jun氨基末端激苏氨酸183／酪氨酸185（JNK—thr183／tyr185）表达。两组比较采用t检验,多组问比较采用单因素方差分析。结果肝脏S6KI基因沉默后,与高脂对照组相比,HFD＋S6K1Ax组小鼠炎性因子MCP-1、TNF-α、IL-1βmRNA均表达下降（分别为0．549±0．016比0．871±0．081、0．635±0．079比0．905±0．059、0．642±0．042比1．327±0．025;t=9．55、6．71、34．07,均P〈0．05）。IL-6mRNA未表现出组间差异（P〉0．05）,抗炎因子IL-10mRNA在HFD＋S6KIAx组肝脏S6K1基因沉默后升高（0．773±0．076比0．436±0．046,t=9．27,P〈0．05）。Western blotting显示与HFD＋pU6Ax组相比,HFD＋S6K1Ax组肝脏S6K1基因沉默后,IRS1－serll01、IRS1-ser636／639、S6K1-thr389、JNK—thr183／tyr185表达下降,Akt—ser473表达增强（t=6．59、8．44、5．37、3．15、6．52,均P〈0．05）。结论高脂喂养可引起肝脏低度炎症并介导胰岛素抵抗的发生,肝脏S6K1可能通过促进炎症因子、抑制抗炎因子表达参与了肝脏胰岛素抵抗发生。     

A Moderately High Fat Diet Promotes Salt-Sensitive Hypertension in Obese Zucker Rats by Impairing Nitric Oxide Production

The objective of this research was to examine the contribution of a moderately high fat (MHF) diet to the development of salt-sensitive hypertension in obese Zucker rats. Lean and obese Zucker rats were fed either a MHF diet or a diet of standard rat chow (control diet) for 10 weeks. From week 4 through week 10, the drinking water was supplemented with 1% NaCl. Blood pressure was measured weekly, and urinary excretion of nitric oxide metabolites (NO_x) was determined at weeks 4 and 10. At week 10, renal nitric oxide synthase (NOS) activity was assessed in kidney homogenates. Blood pressures of obese, but not lean, rats on the MHF fat diet were significantly increased by salt-supplementation, whereas blood pressures of rats on the control diet were not appreciably affected. NO_x excretion was increased in response to salt-supplementation in rats on the control diet, with the effect being particularly dramatic in obese rats. After salt-supplementation, NO_x excretion by rats on the MHF diet was lower than rats on the control diet. In obese rats on the MHF diet, this decrease in NO production was accompanied by a reduction in renal NOS activity. These results indicate that obese rats are more inclined than lean rats to develop diet-induced hypertension in response to a moderately high fat, salt-supplemented diet. Furthermore, they suggest that MHF diet-induced defects in NO production may promote the salt-sensitivity of blood pressure in obese Zucker rats, which appear to require more NO to maintain blood pressure during a salt challenge.     

Lipid Accumulation Product and 25-OH-Vitamin D Deficiency in Type 2 Diabetes

BACKGROUND: Emerging data suggest a link between vitamin D (25(OH)D) deficiency, type 2 diabetes (T2D), and visceral adiposity. The lipid accumulation product (LAP), strictly correlated with abdominal fat depots, is proposed as marker of dysfunctional adiposity. AIM: To verify the association between 25(OH)D levels and LAP in T2D. METHODS: Body mass index (BMI), waist circumference (WC), glucose, HbA1c, lipids, and 25(OH)D were assessed in 420 T2D outpatients and in 150 non-diabetic obese with similar anthropometric characteristics. LAP was computed as the product of sex-specific enlarged WC and triglycerides (TG). RESULTS: In T2D patients, 63.0% showed 25(OH)D deficiency (<20 ng/ml) vs. 71.3% in the obese control group. Overweight males showed a higher prevalence of 25(OH)D deficiency (60.3%) than women (48.8%, p < 0.001), while in obese patients this prevalence was not significant. In both genders, 25(OH)D was not significantly associated with HbA1c and fasting glucose. Age-adjusted 25(OH)D levels were inversely correlated with BMI (p < 0.001), WC (p < 0.001), and LAP (p < 0.001) in both genders. Metabolic syndrome presented an odds ratio (OR) for 25(OH)D deficiency of 1.6 (1.1-2.5, p = 0.048) in females and 1.7 (1.2-2.7, p = 0.016) in males, while the highest quartile of LAP showed an OR of 2.1 (1.2-3.6, p = 0.019) in females and 3.2 (1.6-6.5, p = 0.02) in males. A similar trend was observed in the obese control group. CONCLUSIONS: In the presence of excess weight, subjects with and without T2D frequently feature low 25(OH)D levels. Subjects with higher LAP exhibit a high risk of 25(OH)D deficiency, suggesting that dysfunctional adiposity is a worsening factor for vitamin D hypovitaminosis.     

Elevated plasma fractalkine levels are associated with higher levels of IL-6, Apo-B,LDL-C and insulin,but not with body composition in a large female twin sample

Objective

Plasma fractalkine (FRACT) is involved in the development of numerous inflammatory conditions including atherosclerosis. It is associated with type 2 diabetes mellitus and adipose inflammation. However, whether FRACT is associated with major risk factors for cardiovascular disease, in particular obesity, metabolic syndrome and blood lipids, is virtually unknown.

Methods

The study included a large community-based sample of 3306 middle-aged women drawn from the general UK population. Blood samples were analyzed for circulating levels of FRACT, leptin, insulin, glucose, LDL-C, HDL-C, Apo-A, ApoB and IL-6. Obesity was assessed by fat body mass (FBM) using dual-energy x-ray absorptiometry and by body mass index (BMI).

Results

We found no association between FRACT and body composition, in particular adiposity. Obese and non obese subjects with metabolic syndrome tended to have higher levels of FRACT compared with non-obese subjects without metabolic syndrome but this did not reach statistical significance. Most importantly we report significant correlations between FRACT and circulating IL-6, Apo-B, LDL-C and insulin. The associations with IL-6 and Apo-B were particularly significant (P-value < 0.001), and survived correction for multiple testing and adjustment for age and other covariates.

Conclusion

Higher FRACT levels correlated with elevated levels of IL-6, Apo-B, LDL-C and insulin, all known risk factors for several clinical related diseases suggesting a potential role of FRACT in inflammation and tissue injury. Variations of FRACT levels are not influenced by body composition and are not correlated with leptin indicating that fat mass alone is not responsible for elevation of FRACT seen in obese individuals.     

Measures of body fat in South Asian adults

Background:

South Asian people who originate from the Indian subcontinent have greater percent body fat (%BF) for the same body mass index (BMI) compared with white Caucasians. This has been implicated in their increased risk of type 2 diabetes and cardiovascular disease. There is limited information comparing different measures of body fat in this ethnic group.

Objectives:

The objectives of this study were: (1) to investigate the correlation of %BF measured by a foot-to-foot bioelectrical impedance analysis (FF-BIA) against the BOD POD, a method of air-displacement plethysmography, and (2) to determine the correlations of simple anthropometric measures, (that is, BMI, body adiposity index (BAI), waist circumference (WC), hip circumference (HC) and waist-to-hip ratio (WHR)) against the BOD POD measure of body fat.

Methods:

Eighty apparently healthy South Asian men and women were recruited from the community, and measurements of height, weight, WC, HC and body composition using Tanita FF-BIA and BOD POD were taken.

Results:

The mean±s.d. age of participants was 27.78±10.49 years, 42.5% were women, and the mean BMI was 22.68±3.51 kg m⁻². The mean body fat (%BF) calculated by FF-BIA and BOD POD was 21.94±7.88% and 26.20±8.47%, respectively. The %BF calculated by FF-BIA was highly correlated with the BOD POD (Pearson''s r=0.83, P<0.001), however, FF-BIA underestimated %BF by 4.3%. When anthropometric measures were compared with % BF by BOD POD, the BAI showed the strongest correlation (r=0.74) and the WHR showed the weakest (r=0.33). BAI generally underestimated %BF by 2.6% in comparison with %BF by BOD POD. The correlations of BOD POD with other measures of %BF were much stronger in subjects with a BMI >21 kg m⁻² than those with a BMI ⩽21 kg m⁻².

Conclusion:

The FF-BIA and BAI estimates of %BF are highly correlated with that of BOD POD among people of South Asian origin, although both methods somewhat underestimate % BF. Furthermore, their correlations with % BF from BOD POD are significantly weakened among men and women with a BMI ⩽21 kg m⁻².     

Sonography of fat necrosis of the breast: Correlation with mammography and MR imaging

Fat necrosis (FN) of the breast is a benign nonsuppurative inflammatory process of the adipose tissue. The radiologic appearance ranges from benign to suspicious for malignancy; therefore, it is very important to know the distinguishing radiologic features of FN on different modalities. Mammography is more helpful in identifying FN than ultrasonography in most of the cases, and MRI may also be used to rule out malignancy as an adjunct to mammography and sonography. Even when modern diagnostic modalities are used, biopsy may still be unavoidable for some cases. In conclusion, an accurate history and familiarity with the radiologic findings are crucial to recognizing FN and avoiding unnecessary interventions. © 2013 Wiley Periodicals, Inc. J Clin Ultrasound 41 :415–423, 2013