Surgical metabolism

Summary. Trauma, operative interventions, infection and other disturbances of homeostasis lead to a uniform reaction of the body, namely release and activation of hormones and cytokines. Profound alterations of substrate flow result, with mobilization of energy stores and degradation of structural and functional proteins of vital organs like the gut mucosa. Due to these reactions the energy demands of the organs are met and energy-consuming synthesis of substrates is indicated. Clinically, hypermetabolism, hyperglycemia, lipolysis and increased urea production with negative nitrogen balance can be observed. The metabolic reactivity is reached by an increased substrate cycling. To avoid negative consequences such as organ dysfunction, a rational situation-adapted substrate supply is warranted as well as reduction of catabolic stimuli and stimulation of anabolic factors. The metabolic care of the surgical patient is still a basic and important task.      

Acute actions of insulin-like growth factor II on glucose metabolism in adult rats

Summary The metabolic potency of recombinant human insulin-like growth factor II was studied in anaesthetized adult rats by obtaining dose-response curves for the hypoglycaemic action and for the stimulation of glucose metabolism during euglycaemic clamping. Compared to insulin, about 50 times higher doses of insulin-like growth factor II were required to result in identical in vivo responses, with half-maximally effective serum concentrations for the stimulation of glucose disposal during clamp studies of about 0.8 and 50 pmol/ml, respectively. A similar difference in potency was observed for the dose-dependent stimulatory actions on glucose metabolism in individual target tissues. Half-maximally effective serum concentrations in the range of 0.8 to 3.0 pmol/ml for insulin and of 40 to 70 pmol/ml for insulin-like growth factor II were seen to be required for 2-deoxyglucose uptake, glycogen formation in skeletal muscle and lipogenesis in epididymal fat. Maximal responses were identical with both peptides. These data suggest that in vivo acute metabolic actions of insulin-like growth factor II on carbohydrate metabolism occurred through insulin receptors.     

胃肠道肿瘤病人围手术期细胞因子及蛋白质代谢的变化

目的 :探讨胃肠道肿瘤病人手术后肿瘤坏死因子 α (TNF α)、白介素 6 (IL 6 )、白介素 10 (IL 10 )的变化以及与蛋白质代谢的关系。　方法 :用酶联免疫法 (ELISA)检测 19例胃肠道肿瘤根治术病人术前和术后 1、3、5天血清TNF α、IL 6和IL 10水平 ,同时检测蛋白质分解代谢相关指标、2 4h尿中尿素和肌酐排泄量。　结果 :胃肠道肿瘤根治术后病人TNF α呈下降趋势 ,术后第 1天较术前明显下降 (P <0 .0 5 )。IL 6和IL 10术后升高 (P <0 .0 1) ,尤以术后第 1天升高明显。术后 2 4h尿中尿素和肌酐排泄量明显升高。　结论 :胃肠道肿瘤根治术后病人IL 6和IL 10的升高支持手术应激导致的细胞因子释放变化 ,但TNF α呈下降趋势 ,可能与胃肠道肿瘤病人术前TNF α的高表达有关。术后蛋白质分解代谢增加 ,可能与细胞因子IL 6和IL 10的升高有关。     

The problem of rickets in UK Asians

A large body of work relating to the occurrence of rickets in UK Asians is reviewed. Several theories of the aetiology of this condition are shown to be untenable: it is not exclusively a function of sunlight deprivation or of darker pigmentation; nor is it simply due to phytate-induced losses of calcium from the gut. Asian rickets, however, is associated with a high consumption of cereals, and experiments with rats have suggested a mechanism. In the absence of adequate vitamin D from sunlight, the low-calcium, high cereal intake of the UK Asian population may induce a state of mild secondary hyperparathyroidism which enhances the destruction of vitamin D and leads to a progressive reduction in vitamin D status and, ultimately, to the development of clinical rickets.     

Natural history of parathyroid function and calcium metabolism after kidney transplantation: a single-centre study.

BACKGROUND: The natural history of parathyroid function after successful renal transplantation (RT) and the factors predisposing to persistent hyperparathyroidism (HPT) are not well established. A better knowledge of these data may be helpful in the development of algorithms for optimal surveillance and treatment of HPT after successful RT. Our aim was to evaluate the post-transplant natural history of parathyroid function and calcium metabolism in patients with a functional renal graft and to identify risk factors for persistent HPT. METHODS: Charts of 1165 allograft kidney recipients transplanted between 1989 and 2000 were reviewed. Patients with an intact parathyroid hormone (iPTH) level available at the time of transplantation were identified. The charts of the latter patients were checked for a variety of demographic and clinical data, and all determinations of the iPTH concentration available since transplantation were recorded. Serum levels of calcium, phosphorus, alkaline phosphatases and creatinine, concurrently determined, were also registered. RESULTS: After an initial fall, iPTH levels showed a slow but steady decline towards the upper normal limit. The prevalence of persistent HPT, defined as an iPTH level > or =2.5 times the upper normal limit or the need for parathyroidectomy following transplantation, remained stable at approximately 17% up to 4 years after transplantation. Patients with persistent HPT had significantly elevated serum levels of iPTH, calcium and phosphorus at the time of RT, and had spent a longer time on dialysis. Post-transplant iPTH levels correlated significantly with transplant kidney function. CONCLUSION: Kidney transplant recipients with a high iPTH and calcium x phosphate product at the time of transplantation are at risk for persistent HPT especially when renal function is suboptimal. Therapy for persistent HPT, if considered, should be initiated 3 months post-transplantation since further spontaneous improvement of parathyroid function thereafter is limited.     

Usefulness of osteoprotegerin in assessing responses to neridronate treatment in Paget's disease of bone

Osteoprotegerin (OPG) is a protein that inhibits of osteoclastogenesis. The aim this study was to evaluate the response of serum OPG levels to neridronate treatment in patients with Paget's disease of bone resistant to previous therapy. Nine patients (4 men) affected by active Paget’s disease of bone (6 polyostotic, 3 monostotic) not responsive to clodronate were studied. Serum OPG, osteocalcin, total and bone isoenzyme of alkaline phosphatase (AP and BAP, respectively), and urinary deoxypyridinoline (DPD) were measured before and 5 months after neridronate treatment (100 mg/day, i.v. for two days). A scintigraphic activity index (SAI) was also calculated before treatment. Mean baseline OPG levels were within normal values and were not significantly different 5 months after neridronate treatment. In contrast, there were significant reductions in AP (41.9%, p<0.02) and BAP (38.8%, p<0.04). Serum OPG levels correlated with DPD (r=0.925) and SAI (r=0.689). Although OPG is an important regulator of bone metabolism, in our series of already treated patients it was not a sensitive marker for diagnosing Paget's disease and for monitoring the response to pharmacological treatment, whereas AP and BAP confirmed their clinical usefulness. This preliminary study requires confirmation by a study with a larger population.     

田径运动员最大摄氧量和无氧功测试中血乳酸的应用

目的:研究田径运动员最大摄氧量和Wingate测试后血乳酸的变化,分析血乳酸对测试结果的意义。方法:测试田径短跑运动员36例和中长跑运动员29例的最大摄氧量和Wingate无氧功,以及测试后的血乳酸值。结果:最大摄氧量测试后血乳酸数值为9～11mmol/L左右,摄氧量与乳酸值没有直接相关关系,但不同项目之间有一定的差异;Wingate测试后血乳酸数值一般大于12mmol/L,测试的主要评价指标与乳酸值都有较高的相关关系。结论:血乳酸值对于最大摄氧量测试意义不大,但对于Wingate测试可以作为一项辅助评价指标。     

Monitoring myocardial reperfusion injury with NADH fluorometry.

Using NADH fluorometry to monitor myocardial metabolism, the mechanism of reperfusion injury was investigated after the delivery of an experimental reperfusate. Using an isolated working heart preparation, rat hearts underwent 15 min of global ischemia at 37 degrees C. Following the ischemic insult, an oxygenated enriched reperfusion solution was given for 5 min. The hearts were then returned to a working state and aortic flow recorded to evaluate recovery. NADH levels were monitored throughout the experiment with a fluorometer and glycogen, AMP, ADP, and ATP were measured biochemically pre- and postischemia, after reperfusion and after recovery. In this study, reperfusion injury was best abated by an enriched reperfusate. Our results indicate the mechanism for this amelioration is not high-energy phosphate replenishment. Rather, as indicated by NADH fluorescence, the hearts attain an intermediate level of metabolism that permits glycogen to be restored and functional recovery to be improved.     

Skeletal Muscle Adaptations to Physical Training in Type II (Non-insulin-dependent) Diabetes Mellitus

Seven middle-aged men with manifest type II diabetes mellitus underwent an endurance training programme for 10–15 weeks. The maximal aerobic capacity, as well as the endurance capacity, was improved by 10% (p<0.05). The intramuscular glycogen store increased by more than 80% (p<0.05) from 350 μmol/g dw (dry weight), and the activities of citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase increased by more than 50% (p<0.05) and 30% (p<0.05). The activity of glycogen synthase was decreased by approximately 20% (p<0.05), whereas lactate dehydrogenase remained unchanged. Capillaries/fibre and fibre area increased by more than 50% (p<0.05) and 30% (p<0.05) leaving the area of supply constant. Training did not influence fasting blood lipids and glucose, glycosylated hemoglobin, oral glucose tolerance, and insulin response to an oral glucose load measured 72 hours post-exercise. It is concluded that patients with manifest type II diabetes, as normoglycaemic individuals, adapt to physical training. However, no persistent effect on glucohomeostasis and lipaemia is produced by short-term training in the diabetic patients.