In vivo subcutaneous adipose tissue glucose kinetics after glucose ingestion in obesity and fasting

The kinetic pattern of subcutaneous adipose tissue extracellular glucose following glucose ingestion was investigated in vivo with a microdialysis technique in normal-weight (n = 21) and obese subjects (n = 18) before and after a 7-day fast (n = 9). A dialysis probe (4 x 0.5 mm) was implanted subcutaneously, and was continuously perfused (5 microliters/min). The tissue dialysate glucose concentration was determined in 15-min samples before and during a period of 180 min after a 75-g oral glucose load. A comparison was made between the tissue dialysate concentrations and the venous blood glucose levels. In all study groups the increase in subcutaneous tissue dialysate glucose following glucose ingestion paralleled that in blood, with a time-lag of up to 15 min. In the normal-weight subjects the maximum relative increase in abdominal adipose tissue dialysate glucose was 25% higher (p less than 0.005) than the corresponding blood glucose level, and the total relative glucose level (area under curve, AUC) in abdominal fat was 20% (p less than 0.01) higher than in blood. In contrast, the kinetics of gluteal subcutaneous tissue dialysate and blood glucose levels were similar. In the obese patients before the fasting period the maximum relative glucose level in abdominal fat was almost twice as high as in blood (p less than 0.005), and the total glucose level (AUC) was 50% higher than the blood glucose AUC (p less than 0.005). After the fast, on the other hand, almost identical relative dynamics of abdominal subcutaneous tissue and blood glucose levels were found.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormal regulation of venous alanine after glucose ingestion in myotonic dystrophy

The concentration of amino acids in whole blood was measured before and during standard 5 h oral glucose tolerance testing in six male patients with myotonic dystrophy and five normal males. The plasma levels of insulin and glucose were also determined. From 90 to 240 min after glucose ingestion there was a striking decline in venous alanine concentration in the patients with myotonic dystrophy in contrast to a slight rise in alanine in the normal group. The patients displayed normal glucose tolerance, and there was a sustained fall in the venous concentration of the insulin-sensitive amino acids comparable with that seen in the normal controls. However, the patients showed a threefold increase of plasma insulin after glucose. These data indicate an abnormal regulation of alanine in myotonic dystrophy which may be the result of an alteration in muscle synthesis of this amino acid. This defect in alanine synthesis may be due to a decreased availability of intracellular pyruvate caused by the insulin resistance that exists in these patients.     

Gastric emptying and release of incretin hormones after glucose ingestion in humans.

This study investigated in eight healthy male volunteers (a) the gastric emptying pattern of 50 and 100 grams of glucose; (b) its relation to the phase of interdigestive motility (phase I or II) existing when glucose was ingested; and (c) the interplay between gastric emptying or duodenal perfusion of glucose (1.1 and 2.2 kcal/min; identical total glucose loads as orally given) and release of glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1(7-36)amide (GLP-1), C-peptide, insulin, and plasma glucose. The phase of interdigestive motility existing at the time of glucose ingestion did not affect gastric emptying or any metabolic parameter. Gastric emptying of glucose displayed a power exponential pattern with a short initial lag period. Duodenal delivery of glucose was not constant but exponentially declined over time. Increasing the glucose load reduced the rate of gastric emptying by 27.5% (P < 0.05) but increased the fractional duodenal delivery of glucose. Both glucose loads induced a fed motor pattern which was terminated by an antral phase III when approximately 95% of the meal had emptied. Plasma GLP-1 rose from basal levels of approximately 1 pmol/liter of peaks of 3.2 +/- 0.6 pmol/liter with 50 grams of glucose and of 7.2 +/- 1.6 pmol/liter with 100 grams of glucose. These peaks occurred 20 min after glucose intake irrespective of the load. A duodenal delivery of glucose exceeding 1.4 kcal/min was required to maintain GLP-1 release in contrast to ongoing GIP release with negligibly low emptying of glucose. Oral administration of glucose yielded higher GLP-1 and insulin releases but an equal GIP release compared with the isocaloric duodenal perfusion. We conclude that (a) gastric emptying of glucose displays a power exponential pattern with duodenal delivery exponentially declining over time and (b) a threshold rate of gastric emptying of glucose must be exceeded to release GLP-1, whereas GIP release is not controlled by gastric emptying.     

Effects of ethanol ingestion on maternal and fetal glucose homeostasis

Carbohydrate metabolism has been studied in the offspring of rats fed liquid diet containing ethanol during gestation (EF group). Weight-matched control dams were given liquid diet either by the pair-fed technique (PF group) or ad libitum (AF group). EF and PF dams showed reduced food consumption and attenuated gain in body weight during the gestation period compared with the AF group. Blood glucose, liver glycogen, and plasma insulin levels were significantly reduced in EF and PF dams. Ethanol ingestion resulted in a significant decrease in litter survival and fetal body weight. At term, EF pups on average showed a 30% decrease in blood glucose levels and 40% decrease in plasma insulin levels compared with AF pups. One hour after birth, EF pups exhibited a marked increase in blood sugar level compared with either control group; subsequently, there was a marked decrease in blood glucose levels in EF pups. Liver glycogen stores were significantly reduced in term EF fetuses and were mobilized more rapidly in EF neonates than in either control group. Fetal hyperinsulinemia disappeared shortly after delivery in control pups, as expected; however, in EF pups, the fall in plasma insulin level was gradual. Fetal and neonatal plasma glucagon levels were not altered by ethanol exposure in utero. Blood glucose levels remained significantly low at 2 days of age in EF pups, but reached near control values at 4 days of age. Plasma insulin and glucagon were nearly equal in EF and control pups at 2 and 4 days of age. These results show aberrations in blood glucose, plasma insulin, and liver glycogen levels in offspring exposed to ethanol in utero.     

Acute effects of aerobic exercise intensity on arterial stiffness after glucose ingestion in young men

Arterial stiffness increases after glucose ingestion. Acute low‐ and moderate‐intensity aerobic exercise decreases arterial stiffness. However, the acute effects of 30 min of cycling at low‐ and moderate‐intensity [25% (LE trial) and 65% (ME trial) peak oxygen uptake, respectively] on arterial stiffness at 30, 60 and 120 min of a postexercise glucose ingestion. Ten healthy young men (age, 22·4 ± 0·5 years) performed LE and ME trials on separate days in a randomized controlled crossover fashion. Carotid–femoral (aortic) pulse wave velocity (PWV), femoral–ankle (leg) PWV, carotid augmentation index (AIx) and carotid blood pressure (BP) (applanation tonometry), brachial and ankle BP (oscillometric device), heart rate (HR) (electrocardiography), blood glucose (UV‐hexokinase method) and blood insulin (CLEIA method) levels were measured at before (baseline) and at 30, 60 and 120 min after the 75‐g OGTT. Leg PWV, ankle pulse pressure and BG levels significantly increased from baseline after the 75‐g OGTT in the LE trial (P<0·05), but not in the ME trial. Insulin levels and HR significantly increased from baseline after the 75‐g OGTT in both trials (P<0·05). Aortic PWV, carotid AIx, brachial BP and carotid BP did not change from baseline after the 75‐g OGTT in both trials. The present findings indicate that aerobic exercise at moderate intensity before glucose ingestion suppresses increases leg arterial stiffness after glucose ingestion.     

糖尿病患者糖化血红蛋白与动态血糖关系研究

目的 探讨糖尿病患者糖化血红蛋白与动态血糖关系研究.方法 选取2009～2010年在本院门诊确诊的糖尿病患者120例为研究对象,对所有患者进行血糖和糖化血红蛋白的筛查,然后按照不同的流程进行口服葡萄糖耐受度和糖化血红蛋白(HbA1c)检查.并对其关系进行研究.结果 研究检测结果表明HbA1c与动态血糖之间的关系为正相关,即随着血糖升高,HbA1c也升高.结论 对糖尿病患者的HbA1c实行监控,有利于提高糖尿病控制的全面达标,减少糖尿病慢性并发症的发生率,有着很大的临床诊断价值.     

Differential blood pressure and hormonal effects after glucose and xylose ingestion in chronic autonomic failure

1. To investigate whether carbohydrate contributes to postprandial hypotension in autonomic failure, the cardiovascular, biochemical and hormonal effects of oral glucose and an iso-osmotic solution of oral xylose were studied on separate occasions in six patients with chronic autonomic failure. The effects of oral glucose were also studied in eight normal subjects. 2. In the patients oral glucose lowered blood pressure substantially (-34 +/- 7% at 60 min, area under curve -24.9 +/- 3.5%, P less than 0.001) and for a prolonged period (-25 +/- 4% at 120 min). Plasma noradrenaline levels did not change. In the normal subjects blood pressure was unchanged and plasma noradrenaline rose, suggesting a compensatory increase in sympathetic nervous activity. 3. In the patients xylose caused a smaller and more transient fall in blood pressure (-15 +/- 6% at 90 min, area under curve -8.9 +/- 4%, P less than 0.05) with a non-significant elevation in packed cell volume (36.7 +/- 1.8 to 38.2 +/- 1.8). It was therefore unclear if xylose was exerting osmotic effects within the bowel which contributed to the small blood pressure fall. Packed cell volume did not change in either the patients or normal subjects after glucose. 4. In the patients and normal subjects plasma insulin rose after glucose. Insulin levels were unchanged after xylose. Levels of pancreatic polypeptide and neurotensin, a potential vasodilator, rose in the patients only. The latter rose to a similar extent after both glucose and xylose, making it unlikely that neurotensin alone accounted for the hypotension. 5. These studies indicate that the carbohydrate components of a meal, and in particular those causing insulin release, contribute to postprandial hypotension in patients with autonomic failure.     

Effect of protein ingestion on the glucose and insulin response to a standardized oral glucose load

Type II diabetic subjects were given 50 g protein, 50 g glucose, or 50 g glucose with 50 g protein as a single meal in random sequence. The plasma glucose and insulin response was determined over the subsequent 5 h. The plasma glucose area above the baseline following a glucose meal was reduced 34% when protein was given with the glucose. When protein was given alone, the glucose concentration remained stable for 2 h and then declined. The insulin area following glucose was only modestly greater than with a protein meal (97 +/- 35, 83 +/- 19 microU X h/ml, respectively). When glucose was given with protein, the mean insulin area was considerably greater than when glucose or protein was given alone (247 +/- 33 microU X h/ml). When various amounts of protein were given with 50 g glucose, the insulin area response was essentially first order. Subsequently, subjects were given 50 g glucose or 50 g glucose with 50 g protein as two meals 4 h apart in random sequence. The insulin areas were not significantly different for each meal but were higher when protein + glucose was given. After the second glucose meal the plasma glucose area was 33% less than after the first meal. Following the second glucose + protein meal the plasma glucose area was markedly reduced, being only 7% as large as after the first meal. These data indicate that protein given with glucose will increase insulin secretion and reduce the plasma glucose rise in at least some type II diabetic persons.     

Biphasic patterns of peripheral insulin and glucose levels after lunch in normal subjects

The dynamic relationship of glucose concentrations and insulin secretion during the postabsorptive state is complex and has been associated with a variety of cyclic rhythms. To study the pattern of insulin and glucose response immediately after a mixed meal, we collected blood every 15 min from 0730 to 1645 h from eight normal resting men (age 24.9 +/- 2.1 yr). They took identically constituted mixed meals at 0800 and 1145 h. Concentrations of glucose and insulin were measured in samples taken throughout the study, whereas levels of C-peptide, glucagon, and alpha-NH2 were determined in samples taken after 1130 h only. Computer-assisted analysis was used to identify significant increments and declines in concentrations and to quantify the coincidence of peaks of glucose, C-peptide, glucagon, and alpha-NH2 with peaks of insulin. Coefficients of correlation between data points were calculated for each individual. The patterns of blood insulin and glucose after breakfast and lunch were different. After breakfast, a single simultaneous peak in insulin and glucose occurred approximately 60 min after starting the meal. In contrast, the pattern after lunch in seven of the eight subjects was clearly biphasic. There were secondary, significant coincident peaks in serum insulin, glucose, and C-peptide occurring 1.75-2.25 h after the meal was served. The secondary peak appeared unrelated to the late absorption of protein because it was not associated with consistent changes in serum alpha-NH2 concentration. Erratic variations characterized the postlunch pattern of glucagon levels, excluding a role for this counterregulatory hormone in the control of the biphasic insulin and glucose response.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of obesity on the antilipolytic effect of insulin in isolated human fat cells obtained before and after glucose ingestion.

The antilipolytic effect of insulin was studied in 9 obese and 10 age- and sex-matched subjects of normal weight. Isolated fat cells were taken before and 1 h after an 100 g oral glucose load. Insulin inhibition of basal and isoprenaline-induced rates of lipolysis were determined by using a sensitive bioluminescent glycerol assay. When compared with the controls, the obese group showed a lower glucose tolerance, a higher insulin secretion, and a lower specific insulin receptor binding per adipocyte surface area, which would suggest an insulin-resistant state. Before oral glucose, however, the sensitivity of the antilipolytic effect of insulin was enhanced 10-fold in obesity (P less than 0.01), but the maximum antilipolytic effect was not altered. Glucose ingestion induced a 10-25-fold increase in insulin sensitivity (P less than 0.01) and a 10% but not significant increase in specific adipocyte insulin receptor binding in the nonobese group. In the obese group, however, neither the insulin binding nor the antilipolytic effect of the hormone was increased by oral glucose. After oral glucose, insulin sensitivity was similar in the two groups. The concentration of the hormone which produced a half maximum effect was about 1 microU/ml. Similar results were obtained with insulin inhibition of basal and isoprenaline-stimulated glycerol release. It is concluded that, after an overnight fast, the sensitivity of the antilipolytic effect of insulin is markedly enhanced in adipocytes of "insulin-glucose resistant" obese subjects, presumably because of alterations at postreceptor levels of insulin action. In obesity, the antilipolytic effect of insulin seems normal after glucose ingestion. Furthermore, in adipocytes of subjects of normal weight, oral glucose rapidly stimulates the sensitivity of the antilipolytic effect of insulin, apparently because of changes at postreceptor sites. This short-term regulation of insulin action following the ingestion of glucose does not seem to be present in obesity.     

Mechanisms of postprandial glucose counterregulation in man. Physiologic roles of glucagon and epinephrine vis-a-vis insulin in the prevention of hypoglycemia late after glucose ingestion.

The transition from exogenous glucose delivery to endogenous glucose production late after glucose ingestion is not solely attributable to dissipation of insulin and, therefore, must also involve factors that actively raise the plasma glucose concentration--glucose counterregulatory factors. We have shown that the secretion of two of these, glucagon and epinephrine, is specific for glucose ingestion and temporally related to the glucose counterregulatory process. To determine the physiologic roles of glucagon and epinephrine in postprandial glucose counterregulation, we produced pharmacologic interventions that resulted in endogenous glucagon deficiency with and without exogenous glucagon replacement, adrenergic blockade, and adrenergic blockade coupled with glucagon deficiency starting 225 min after the ingestion of 75 g of glucose in normal subjects. Also, we assessed the effect of endogenous epinephrine deficiency alone and in combination with glucagon deficiency late after glucose ingestion in bilaterally adrenalectomized subjects. Glucagon deficiency resulted in nadir plasma glucose concentrations that were approximately 30% lower (P less than 0.01) than control values, but did not cause hypoglycemia late after glucose ingestion. This effect was prevented by glucagon replacement. Neither adrenergic blockade nor epinephrine deficiency alone impaired the glucose counterregulatory process. However, combined glucagon and epinephrine deficiencies resulted in a progressive fall in mean plasma glucose to a hypoglycemic level late after glucose ingestion; the final glucose concentration was 40% lower (P less than 0.02) than the control (epinephrine deficient) value in these patients, and was nearly 50% lower (P less than 0.001) than the control value and approximately 30% lower (P less than 0.05) than the glucagon-deficient value in normal subjects. We conclude (a) the transition from exogenous glucose delivery to endogenous glucose production late after glucose ingestion is the result of the coordinated diminution of insulin secretion and the resumption of glucagon secretion. (b) Epinephrine does not normally play a critical role in this process, but enhanced epinephrine secretion compensates largely and prevents hypoglycemia when glucagon secretion is deficient.     

Stridor after ingestion of dettol and domestos.

Dettol (4.8% chloroxylenol, 9% pine oil and 12% isopropyl alcohol) has previously been reported to cause delayed upper airway obstruction when ingested, despite the product being labelled as non-poisonous. Domestos (1-5% sodium hypochlorite) is used as a household and toilet cleaner. This paper reports a rare case in which both agents were consumed together in significant quantities, and caused stridor and impending airway obstruction requiring endotracheal intubation in the emergency department. Patients who have ingested this combination of cleaning agents are at high risk of acute airway compromise, and should have expert upper airway evaluation and control as soon as possible after admission.     

Influence of glucose and fructose ingestion on the capacity for long-term exercise in well-trained men

Summary. The aim of the present study was to examine the influence of glucose and fructose ingestion on the capacity to perform prolonged heavy exercise. Eight well-trained healthy volunteers exercised on a bicycle ergometer at 68±3% of their VO₂ max until exhaustion, on three occasions, with 8-day intervals. During the exercise they ingested either glucose (250 ml, 7%), fructose (250 ml, 7%) or water (250 ml) every 20 min in a double-blind randomized study design. Arterial blood samples were collected at rest and during exercise for the determination of substrates and hormones. Muscle glycogen content (m. quadriceps femoris) was measured before and after exercise. The duration of exercise lengthened with repeated exercise (3rd test: 136±13 min v. 1st test: 110±12 min, P<0·01). Corrected for the sequence effect, total work time until exhaustion was significantly longer with glucose (137±13 min) than with either fructose (114±12 min) or water (116±13 min) (both P<0·01). When glucose or fructose was ingested, the arterial plasma glucose concentration was maintained at the normoglycaemic level; with water ingestion, plasma glucose values fell during exercise in seven subjects and remained at the resting level in the eighth subject. The muscle glycogen concentration was 467±29 mmol kg d.w.^-1 at rest and fell to approximately half the initial value at exhaustion. In the subgroup of seven subjects in whom glucose values decreased with water intake, the mean rate of glycogen degradation was significantly lower (P<0·05) with the ingestion of glucose (1·3±0·4 mmol kg d.w.^-1 min^-1) as compared to fructose (2·1±0·5 mmol kg d.w.^-1 min^-1) or water (2·3±0·5 mmol kg d.w.^-1 min^-1). Intermittent glucose ingestion (3×17·5 g h^-1) during prolonged, heavy bicycle exercise postpones exhaustion and exerts a glycogen-conserving effect in the working muscles. In contrast, fructose ingestion during exercise maintains the glucose concentration at the basal level but fails to influence either muscle glycogen degradation or endurance performance.     

耳穴埋豆联合中药穴位贴敷预防妇科术后恶心呕吐的效果观察

目的：观察耳穴埋豆联合中药穴位贴敷预防妇科术后恶心呕吐（ PONV）的效果。方法选择2011年12月至2012年11月开腹行妇科三类手术的患者作为观察组,2010年12月至2011年11月行同类手术的患者作为对照组。观察组患者给予双侧耳穴（胃、脾、交感）埋豆按压联合吴茱萸调生姜汁双侧内关穴贴敷,对照组术前未给予特殊的预防恶心呕吐的措施,术后如出现呕吐,则给予药物注射对症处理。观察两组患者术后24 h PONV发生率及严重程度。结果观察组44例中发生PONVⅠ级30例（68．18％）,Ⅱ级4例（9．09％）,Ⅲ级10例（22．73％）;对照组52例患者中,发生 PONVⅠ级23例（44．23％）,Ⅱ级7例（13．46％）,Ⅲ级22例（42．31％）,两组患者PONV发生率比较,差异有统计学意义（Uc ＝2．3322,P＜0．05）。观察组恶心呕吐程度轻,PONV Ⅲ级时经单一用药均能缓解。结论耳穴埋豆联合中药穴位贴敷能降低妇科PONV的发生率,护士易于操作,可在临床推广应用。     

Caffeine ingestion is associated with reductions in glucose uptake independent of obesity and type 2 diabetes before and after exercise training

OBJECTIVE: We investigated the effect of caffeine ingestion on insulin sensitivity in sedentary lean men (n = 8) and obese men with (n = 7) and without (n = 8) type 2 diabetes. We also examined whether chronic exercise influences the relationship between caffeine and insulin sensitivity in these individuals. RESEARCH DESIGN AND METHODS: Subjects underwent two hyperinsulinemic-euglycemic clamp procedures, caffeine (5 mg/kg body wt) and placebo, in a double-blind, randomized manner before and after a 3-month aerobic exercise program. Body composition was measured by magnetic resonance imaging. RESULTS: At baseline, caffeine ingestion was associated with a significant reduction (P < 0.05) in insulin sensitivity by a similar magnitude in the lean (33%), obese (33%), and type 2 diabetic (37%) groups in comparison with placebo. After exercise training, caffeine ingestion was still associated with a reduction (P < 0.05) in insulin sensitivity by a similar magnitude in the lean (23%), obese (26%), and type 2 diabetic (36%) groups in comparison with placebo. Exercise was not associated with a significant increase in insulin sensitivity in either the caffeine or placebo trials, independent of group (P > 0.10). CONCLUSIONS: Caffeine consumption is associated with a substantial reduction in insulin-mediated glucose uptake independent of obesity, type 2 diabetes, and chronic exercise.     

耳穴贴压加穴位按摩对剖宫产术后母乳喂养的影响

目的探讨耳穴贴压加穴位按摩对剖宫产术后母乳喂养的影响。方法将106例剖宫产术后初产妇随机分为试验组57例和对照组49例,两组产妇均按剖腹产术后常规护理,实施母婴皮肤早接触、早吸吮,母婴分离不超过1h,试验组在此基础上给予耳穴贴压加穴位按摩。结果试验组产妇泌乳量较对照组产妇充足;新生儿喂乳次数较对照组新生儿少,两组比较,差异具有统计学意义(均P0.05);试验组新生儿代乳品的使用比例低于对照组新生儿,3个月和4个月新生儿使用代乳品添加情况比较,差异具有统计学意义(均P0.05)。结论耳穴贴压加穴位按摩能促进剖宫产术后产妇乳汁分泌,减少代乳品的使用比例,提高纯母乳喂养率;其操作安全、方便、易被产妇接受,值得临床推广应用。