Electrogastrographic characteristics in patients of stomach cancer

Using a homemade electrogastrography (EGG) system, we studied the characteristics of myoelectrical rhythm in gastric cancer (GC) patients. Based on a short-term Fourier transform, recorded slow waves could be automatically analyzed to obtain the following parameters: dominant frequency/power, percent of normal rhythm (2.4–3.7 cpm), power ratio, etc. Fifty histologically confirmed GC patients (34 men, 16 women) were enrolled before surgical intervention to measure their fasting and postprandial EGG parameters for 30 min. The cancerous parameters of GC patients were then obtained postoperatively. In addition, 46 healthy subjects were enrolled for comparison. When compared to controls, GC patients had the following characteristics: absence of postprandial increase in dominant frequency (GC: 3.04 ± 0.47 vs 3.07 ± 0.44 cpm, NS; controls: 3.02 ± 0.31 vs 3.21 ± 0.25 cpm, P < 0.001), marked power response after meal (P < 0.05), and obvious power ratio (4.58 ± 7.38 vs 2.27 ± 2.05, P < 0.05). Multivariate analysis indicated that advanced GC was the factor responsible for the obvious dominant power enhancement after meal (P < 0.05). Other demographic, clinical, and cancerous factors did not influence EGG parameters. We conclude that apparent arrhythmia is not encountered in GC patients, although they mainly exhibit obvious postprandial power response. Advanced GC is likely responsible for this power enhancement on EGG recording.     

Effects of trimebutine maleate on gastric motility in patients with gastric ulcer

The effects of trimebutine maleate (TM), a prokinetic drug, on gastrointestinal motility in patients with gastric ulcer were investigated. Twenty patients with active gastric ulcers were allocated to two groups; 10 patients received a proton pump inhibitor alone (PPI group), given orally, and 10 patients received oral TM in combination with a PPI (PPI + TM group), each for a period of 8 weeks. Electrogastrography (EGG) and gastric emptying were measured before and after the treatment period. During the active ulcer stage, tachygastria (more than 0.06 Hz) or bradygastria (less than 0.04 Hz) in the EGG frequency were observed in 9 patients either before or after meals. During the healed ulcer stage, tachygastria or bradygastria was observed in 4 of 10 patients in the PPI group, while in the PPI + TM group, 1 patient had tachygastria and none had bradygastria. Postprandial dip (PD) was observed in 3 of the 20 patients during the active stage, while after treatment, PD was observed in 3 patients in the PPI group and in 6 patients in the PPI + TM group, respectively. Gastric emptying in the PPI group did not show any change between before and after treatment, while that in the PPI + TM group improved significantly after treatment. These results suggest that TM may have an ameliorative effect on abnormal gastric motility in patients with gastric ulcer. (Received Sept. 17, 1997; accepted Apr. 24, 1998)     

Role of sham feeding in postprandial changes of gastric myoelectrical activity

The aim of this study was to evaluate the role of sham feeding in postprandial changes of gastric myoelectrical activity. Eighteen asymptomatic healthy volunteers (10 men, 8 women; mean age: 31), with no history of gastrointestinal disease were studied. Gastric myoelectrical activity was recorded for 30 min at baseline, 30 min after sham feeding, and 1 hr after eating, using surface electrogastrography. The electrogastrogram (EGG) was analyzed by spectral analysis. It was found that the changes of postprandial EGG parameters were significantly correlated with those after sham feeding (EGG dominant power:r=0.6,P<0.01; dominant frequency:r=0.8,P<0.001; percentage of regular slow waves:r=0.7,P<0.003). We concluded that intrinsic gastric electrical activity can be altered by sham feeding and the cephalic phase of digestion plays an important role in the postprandial response of gastric myoelectrical activity.     

肝衰竭大鼠胃动力的改变及其机制的初步探讨

[目的]观察肝衰竭大鼠胃动力的变化并探讨其初步机制。[方法]40只Wistar大鼠随机分为肝衰竭模型组和对照组,采用葡聚糖蓝-2000为标记物观察大鼠胃排空的变化,应用乙酰胆碱酯酶(AchE)和NADPH-d组织化学染色(NOS)及肌间神经丛全层铺片技术,观察肝衰竭大鼠胃窦肌间神经丛胆碱能和氮能神经的变化,免疫组化染色观察胃窦C-kit阳性Cajal间质细胞的变化,并进行定量分析。[结果]与对照组比较,模型组大鼠胃排空明显减弱,胃窦肌间神经丛胆碱能阳性神经元数量减少、神经纤维变细、分布较稀疏,2组比较差异有统计学意义(P<0.01);模型组氮能神经阳性神经元数量及神经纤维分布明显高于对照组(P<0.01);胃窦C-kit阳性Cajal间质细胞明显少于对照组(P<0.01)。[结论]肝衰竭大鼠胃动力明显减退,其机制与胃窦肌间神经丛胆碱能神经分布减少、Cajal间质细胞减少及氮能神经分布增加有关。     

Single oral dose of cisapride accelerates gastric antral emptying in healthy humans: An ultrasonographic study

An ultrasonographic study of ten healthy volunteers was carried out to evaluate the effect of cisapride on gastric antral emptying. More than 1 week after the measurement of the baseline emptying rate, cisapride was given at a single oral dose of 5 mg 30 minutes before intake of a balanced liquid test meal (5 ml/kg body weight). To determine the time to half emptying (T1/2), an exponential curve was extrapolated for the elimination phase of the gastroantral sagittal cross-sectional area plotted against time. The T1/2 was reduced by 18.5% after cisapride, from 62.6±4.3 to 51.0±4.4 min (P=0.0284). We conclude that a single oral dose of 5mg of cisapride significantly accelerates the gastric antral emptying rate in healthy humans.     

Ultrasonographic assessment of gastric motility in diabetic gastroparesis before and after attaining glycemic control

Background Glycemic control is important for maintaining gastric motility in diabetic patients, but gastric motility has not yet been studied ultrasonographically in relation to glycemic control.Methods We made such observations before and after establishing glycemic control in diabetic patients with gastroparesis. We studied 30 diabetic patients with upper abdominal digestive symptoms who were hospitalized for correction of poor blood sugar control and who underwent upper digestive tract endoscopy to rule out structural causes such as gastric/duodenal lesions. Gastric motility was evaluated by transabdominal ultrasonography, using a test meal, before and after attainment of glycemic control (within 3 days after admission and 3 days before discharge). Also, upper abdominal digestive symptoms present on admission and at discharge were compared.Results After glycemic control was established, contractions of the antral region were more frequent than before the attainment of control (8.93 ± 1.17/3 min vs 7.63 ± 2.22/3 min, respectively; P < 0.001). Glycemic control also significantly improved gastric emptying (before glycemic control, 49.2 ± 14.8%; after, 67.1 ± 11.5%; P < 0.001). This was also true for the motility index, concerning antral gastric contractility (before control, 2.97 ± 1.57; after, 3.75 ± 1.09; P < 0.05). Upper abdominal symptom scores were also significantly lower after attainment of control than before (0.47 ± 0.78 vs 3.17 ± 2.00, respectively; P < 0.001).Conclusions These findings suggest that attaining glycemic control improves gastric motility and attainments upper abdominal symptoms in diabetic patients with gastroparesis.     

Role of cholecystokinin in the regulation of liquid gastric emptying and gastric motility in humans: studies with the CCK antagonist loxiglumide

Background—Exogenous cholecystokinin (CCK)inhibits antral motility and slows gastric emptying (GE) but the effectof endogenous CCK on the gastric motor mechanisms responsible for GEremains unclear.
Methods—The effect of the CCK-A antagonistloxiglumide (LOX) on GE and motility was studied using magneticresonance imaging in six healthy volunteers after ingestion of 500 mlIntralipid 10% (550 kcal). Subjects were studied in the supineposition on two occasions during intravenous infusion of LOX(66 µmol/kg/h for 10 min followed by 22 µmol/kg/h) or placebo. GEwas determined every 15 minutes using transaxial abdominal scans andmotility was studied by means of 120 coronal scans, 1.2 seconds apart. For each coronal image the proximal and distal (antral) diameters weremeasured at a fixed point in the stomach to determine contraction frequency (ACF) and amplitude (AMP).
Results—GE was faster during LOX infusion thanplacebo (t_1/2 31 (22) versus 115 (67) minutes, p<0.03).There was little variation in the diameter of the proximal stomach witheither LOX or placebo. In the distal stomach marked contractileactivity was observed during LOX (ACF 2.9 (0.2) versus 1.5 (2.9) duringplacebo, p<0.01). AMP also increased during LOX compared with placebo(56 (22)% versus 27 (16)%, p<0.001).
Conclusion—The increases in antral motility arelikely to contribute to the acceleration of GE and suggest that CCK mayregulate GE by acting on the distal stomach although an effect on theproximal stomach cannot be excluded.

Keywords:loxiglumide; magnetic resonance imaging; gastricemptying; gastric motility; antral contraction

     

Gastric motility is an important factor in the pathogenesis of indomethacin-induced gastric mucosal lesions in rats

Effects of atropine, cimetidine, and 16,16-dimethyl prostaglandin E₂ (16,16-dmPGE₂) on indomethacin-induced gastric lesions were investigated in rats by correlating their effects on gastric acid and HCO^}-₃ secretion and motility. Subcutaneously administered indomethacin (25 mg/kg) produced gastric mucosal lesions within 4 hr. In parallel studies, an equivalent dose of indomethacin inhibited gastric HCO^}-₃ secretion, and stimulated gastric motor activity measured as intraluminal pressure recordings, whereas acid secretion was unaffected. The lesions induced by indomethacin were significantly prevented by three agents: cimetidine (100 mg/kg), which reduced acid secretion; atropine (1 mg/kg), which reduced acid secretion and gastric motility; and 16,16-dmPGE₂ (10 g/kg), which reduced acid secretion and motility and increased gastric HCO^– ₃ secretion. If acid (150 mM HCl) was infused into the stomach (1.2 ml/hr) during indomethacin treatment, only the latter two agents significantly prevented the formation of gastric lesions in response to indomethacin. Since only the effect on gastric motility was common to these two agents (atropine and 16,16-dmPGE₂), the increased gastric motility may be an important pathogenetic factor in indomethacin-induced gastric lesions. The presence of acid as well as a deficiency of endogenous PGs may be prerequisite for later extension of the lesions but cannot account for the induction of mucosal lesions in rats following administration of indomethacin.     

Gastric emptying of solids but not liquids is decreased in rats with chronic renal failure

Severe gastric complications occur in uremic patients, yet few studies have addressed the effect of chronic renal failure (RF) on gastric physiology. In the present study, we investigated: (1) the effect of RF on gastric emptying of liquids and solids in awake rats, (2) the motor function in the gastric corpus, and (3) the role of nitric oxide in any alterations in gastric motor function in uremic rats. RF was induced by partial kidney infarction. RF had no effect on gastric emptying of liquids but significantly inhibited gastric emptying of solids by 68%.N-Nitro-l-arginine, an inhibitor of nitric oxide (NO) synthesis, had no effect on the reduced gastric emptying of solids in RF rats. RF rats showed an altered pattern of gastric motility compared to sham-operated rats. These data suggest that RF induced an inhibition of gastric emptying of solids, but not liquids. However, NO does not seem to play a role in this inhibition.This work was supported by NIH grant DDK 41004 (H.E.R.) and the CURE/UCLA Digestive Disease Core Center DDK 41031 (Animal and Gastrointestinal Blood Flow Cores). E.Q. was the recipient of a Fogarty International Fellowship Award (NIH 1 FO5 TWO4443-01) and a grant from the Conserja de Education, Cultura y Deportes of the Canary Islands Autonomous Government. J.B. was supported by a grant from Fondacio La Caixa, Spain.     

Effect of prepyloric gastric transection and anastomosis on sphincter of Oddi cyclic motility in conscious dogs

Purpose. We previously reported significant changes in sphincter of Oddi cyclic motility after proximal duodenal transection and anastomosis. However, the role of intrinsic myoneural continuity between the antrum and duodenum in this respect is not understood. The aim of this study was to elucidate the effects of prepyloric gastric transection on sphincter of Oddi motility in animals in the conscious state. Methods. Pressures in the bile duct, duodenum, stomach, and sphincter of Oddi and their response to an injection of cholecystokinin-octapeptide were measured in four conscious dogs, with a duodenal cannula, before and after gastric transection and anastomosis 1.5 cm proximal to the pylorus. Results. Gastric transection did not affect the initiation and propagation of the gastroduodenal migration motor complex. Biliary pressure (5.7 ± 0.15 to 5.5 ± 0.2 mmHg; P = 0.91), sphincter of Oddi basal pressure (10.6 ± 0.3 to 10.7 ± 0.2 mmHg; P = 0.97), and amplitude (26.0 ± 1.2 to 32.9 ± 1.7 mmHg; P = 0.304) did not change after gastric transection. Biliary pressure decreased from phase II to phase III of the duodenal migrating motor complex. Cholecystokinin-octapeptide inhibited sphincter of Oddi phasic waves before and after gastric transection. Conclusions. Intrinsic myoneural transection at the prepyloric region does not influence sphincter of Oddi cyclic motility. Preservation of pyloroduodenal myoneural continuity in pylorus-preserving gastrectomy would be beneficial to maintain normal sphincter of Oddi motility. Received: October 30, 2000 / Accepted: February 23, 2001     

Postischemic intestinal motility in rat is inversely correlated to length of ischemia

An inverse correlation between postischemic gastrointestinal motility and the length of intestinal ischemia was found in an animal model. Intestinal ischemia was caused without concurrent laparotomy and for a predetermined time period (ischemia time) by pulling on an external nylon thread that was threaded through a double-lumen catheter. This catheter was passed into the abdominal cavity to encircle the superior mesenteric artery. Gastrointestinal motility was determined by the introduction of a color-marked meal into the animal's stomach and the measurement of the proportionate length of the small bowel filled with it (transit index). This simple and reliable animal model can also be used for the evaluation of techniques and pharmacological manipulations aimed at modulation of the effects of intestinal ischemia on intestinal motility and its consequences.     

Endogenous oestradiol but not testosterone is related to coronary artery disease in men

Objectives Men die of coronary artery disease (CAD) more often than women. There is evidence that testosterone either is neutral or has a beneficial effect on male cardiovascular disease. The role of oestrogens in male CAD has been less studied. This study was carried out with the purpose of evaluating the relationship between sex hormone levels and CAD. Design Case–control study. Participants Men (aged 40–70) submitted to coronary angiography. A 70% occlusion of at least one major coronary artery defined the cases; subjects with ≤50% occlusion constituted the control group. Measurements Blood samples were collected for total testosterone (TT), oestradiol, luteinizing hormone, follicle‐stimulating hormone, sex hormone‐binding globulin, lipid profile and albumin measurements. Bioavailable and free testosterone, free androgen index (FAI) and free oestrogen index (FEI) were calculated. Oestradiol and TT levels were examined as terciles, based on the whole study population. Results Of the 140 patients included, 72 were cases and 68 were controls. The baseline characteristics of the two groups were similar, except for the older age and lower LDL‐C in the cases. Oestradiol and FEI but not total, bioavailable and free testosterone and FAI correlated positively with CAD. After adjustments for potential confounders, oestradiol remained statistically significant. The prevalence of CAD was significantly higher in the 3rd than in the 1st tercile of oestradiol. Conclusion In this study, men with CAD had higher oestradiol and FEI levels. Additional studies are needed to clarify the direction of causality and possible underlying mechanisms.     

Relation between histologic gastritis and gastric motility in Japanese patients with functional dyspepsia: evaluation by transabdominal ultrasonography

BACKGROUND: Whether mucosal inflammation affects gastric motility in patients with functional dyspepsia (FD) is controversial. Few reports discuss gastric motility in relation to histologic gastritis. We examined the relation between gastric motility and histologic gastritis in Japanese patients with FD. METHODS: Subjects were 198 patients examined by ultrasonography (US) and endoscopic biopsy. Histologic gastritis scores were compared to three US gastric motility indices: the motility index (MI), gastroduodenal reflux index (RI), and gastric emptying rate (GER). In cases of gastritis with a high inflammation score (score 2-3), the macrophages in biopsy specimens were counted and compared to the motility indices. RESULTS: Of the 198 patients, 159 were Helicobacter pylori positive. Comparison of 39 age-and sex-matched H. pylori-positive and 39 H. pylori-negative patients showed that the MI was lower in H. pylori-positive patients (6.78+/-2.17 vs. 7.63+/-2.35, P<0.05), and the RI was higher (5.64+/-4.70 vs. 2.13+/-2.58, P<0.01). Among H. pylori-positive patients, US revealed a decreased MI in patients with a high inflammation score (score 2-3) in the antrum compared with the MI of those with a low inflammation score (score 0-1) (6.52+/-2.38 vs. 7.82+/-1.89, P<0.01). The number of macrophages was not associated with motility indices in patients with a high inflammation score. CONCLUSION: Histologic gastritis with severe inflammation may inhibit gastric motility.     

Cognitive dysfunction follows left heart catheterisation but is not related to microembolic count

Background

Left heart catheterisation with coronary angiography (CA) may lead to cognitive dysfunction, as a result of neurological injury. The aim was to assess the incidence of cognitive dysfunction in elderly patients three months after CA and investigate any association between cognitive dysfunction and microembolic count during CA.

Methods

This was a prospective observational study with a control cohort. Cognitive testing was undertaken at baseline and at 3 months using a battery of 8 neuropsychological tests. Subjects comprised 51 CA patients, aged ≥ 50 years, with normal baseline cognition, and 31 community control participants. Microemboli were measured by Transcranial Doppler throughout the procedure. All patients underwent trans-femoral CA with aortography and ventriculography. Cognitive dysfunction was defined in an individual when their reliable change index score was less than − 1.96 on 2 or more tests and/or their combined z score was less than − 1.96. Microembolic count was assessed by off-line manual counting and automatic software was also used to count and differentiate gaseous from solid microemboli.

Results

Cognitive dysfunction was identified in 15.7% of patients at 3 months. Microemboli were detected in all patients, predominantly during aortography and ventriculography. The median total embolic count was 365 (IQR 192, 574), the majority being gaseous (84%). There was no multivariable association between cognitive dysfunction at 3 months and microembolic count.

Conclusions

This study demonstrated that cognitive dysfunction following CA is not associated with microembolic load. Cognitive dysfunction occurs in 15.7% of patients at 3 months. This is reassuring for the proceduralist and suggests that other perioperative elements are involved.     

Gastric juice ascorbic acid is related to Helicobacter pylori infection but not ethnicity

BACKGROUND: Maori and Pacific Island ethnic groups in New Zealand have a high risk for gastric cancer. Low levels of gastric juice ascorbic acid (vitamin C) have been suggested to be a risk factor for gastric cancer. Previous studies have shown that gastric juice ascorbic acid may be independently associated with both ethnicity and Helicobacter pylori infection. This study aimed to examine the interrelationship between H. pylori and ethnicity in New Zealand. METHODS: Gastric juice was collected into 70% perchloric acid preservative and stored at -80 degrees C. Ascorbic acid was analysed by high-performance liquid chromatography using ion-pair chromatography and electrochemical detection. Inflammation and atrophy was graded from biopsies from multiple sites in the antrum and body. Gastric juice was collected from 89 patients during routine endoscopy. RESULTS: There was a wide range of measured gastric juice ascorbic acid from 0.001 to 410 microg/mL. The median concentration of ascorbic acid for H. pylori-negative patients was 1.78 microg/mL (n = 57) and 0.12 microg/mL (n = 32) for H. pylori-positive patients (P = 0.001). Gastric juice ascorbic acid concentration was not associated with age, endoscopic diagnosis or intestinal metaplasia, but was significantly associated with the degree of acute inflammation (P = 0.01) and the presence of atrophy (P = 0.04).The median ascorbic acid concentration for European patients was 0.92 microg/mL (n = 44) and 0.09 microg/mL (n = 38) for Maori and Pacific Island ethnic groups combined (P = 0.1). Multiple step-wise regression analysis showed that only H. pylori infection was a significant factor for predicting ascorbic acid concentrations (r2 = 0.12). CONCLUSIONS: This study has confirmed that gastric juice ascorbic acid concentration is lower in the presence of H. pylori infection.     

旋覆代赭汤对胃动力低下大鼠胃窦组织中脑肠肽受体mRNA表达的影响

[目的]观察旋覆代赭汤对胃动力低下大鼠胃窦平滑肌细胞促胃液素受体（GASR）及血管活性肠肽2受体（VIPR2）mRNA表达的影响。[方法]将70只大鼠随机分为正常组和模型组,正常组10只,模型组60只。模型组每只大鼠按10 g/kg体重的甘草煎剂灌胃后,随机分为模型3 d、模型7 d组,旋覆代赭汤低、中、高剂量组及多潘立酮组。多潘立酮组予0.27 mg/ml的多潘立酮混悬液灌胃,旋覆代赭汤低、中、高剂量组分别予浓度为0.369、0.738、1.476 g/ml的旋覆代赭汤灌胃,给药5 d。采用原位杂交法检测大鼠胃窦平滑肌细胞GASR及VIPR2 mR-NA的表达。[结果]一定剂量甘草煎剂可复制大鼠胃动力低下模型,旋覆代赭汤可使胃动力低下大鼠胃窦平滑肌细胞GASR mRNA的阳性细胞平均光密度升高,平均灰度值降低;而VIPR2 mRNA的阳性细胞的平均光密度降低,平均灰度值升高（P〈0.05或〈0.01）。[结论]旋覆代赭汤可通过调节脑肠肽受体在胃窦组织中的表达达到促胃动力的作用。     

Nitric oxide production decreases after salt loading but is not related to blood pressure changes or nitric oxide-mediated vascular responses

BACKGROUND: Nitric oxide production is a homeostatic mechanism that may regulate blood pressure during salt loading. Salt-sensitive hypertension in animal models and in humans is characterized by increased blood pressure and decreased nitric oxide production after salt loading. It is not known if this impaired nitric oxide production is the result of hypertension or is a mechanism contributing to the blood pressure response to salt. METHODS AND RESULTS: The effects of salt loading on blood pressure, nitric oxide-mediated vasodilation and nitric oxide production were measured in 25 normotensive subjects after 6 days on either a high (400 mmol/day) or low (10 mmol/day) sodium, low nitrate diet. Mean arterial pressure increased during the high-salt diet [4 +/- 1 mmHg (mean +/- SEM)] in 12 subjects and remained unchanged or decreased (-4 +/- 1 mmHg) in 13 subjects. Plasma nitrite and nitrate, a measure of nitric oxide production, decreased significantly from 39 +/- 3.3 micromol/l during the low-salt diet to 22.4 +/- 2.4 micromol/l during the high-salt diet (P = 0.0001). However, changes in mean arterial pressure from low- to high-salt diet did not correlate with changes in plasma nitrite and nitrate (r = 0.14, P = 0.51). Forearm blood flow increased significantly (P <0.0001) in response to mental stress, a nitric oxide-mediated response, but was not affected by sodium intake (from 7.8 +/- 0.9 to 11.2 +/- 1.4 ml/min per 100 ml during low salt versus 8.5 +/- 1.2 to 10.4 +/- 1.3 ml/min per 100 ml during high salt,P = 0.3). CONCLUSIONS: Salt loading results in a decrease in nitric oxide production in both salt-sensitive and salt-resistant normotensive subjects, which is independent of changes in blood pressure and does not affect the nitric oxide-mediated vascular response to mental stress. In contrast to salt-resistant animal models, salt loading in healthy subjects does not increase nitric oxide production. Therefore, the increased blood pressure response to salt loading may occur through mechanisms other than nitric oxide, or salt-sensitive individuals are more sensitive to the reduced nitric oxide production that occurs after salt loading in both salt-sensitive and salt-resistant subjects.     

Adiponectin in umbilical cord blood is inversely related to low-density lipoprotein cholesterol but not ethnicity

CONTEXT: Adiponectin is a recognized protective risk marker for cardiovascular disease in adults and is associated with an optimal lipid profile. The role of adiponectin at birth is not well understood, and its relationship with the neonatal lipid profile is unknown. Because ethnic disparities in cardiovascular risk have been attributed to low adiponectin and its associated low high-density lipoprotein cholesterol (HDL-C), investigation at birth may help determine the etiology of these risk patterns. OBJECTIVE: Our objective was to investigate the relationship between neonatal adiponectin and lipid profile at birth in two ethnic groups in cord blood. DESIGN, SETTING, AND PARTICIPANTS: Seventy-four healthy mothers and their newborns of South Asian and White European origin were studied in this cross-sectional study at St. Mary's Hospital, Manchester, United Kingdom. MAIN OUTCOME MEASURES: Serum adiponectin, total cholesterol, HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglyceride levels were measured in umbilical venous blood at birth and in maternal blood collected at 28 wk gestation. RESULTS: Cord adiponectin was significantly inversely associated with cord LDL-C (r = -0.32; P = 0.005) but not HDL-C. In a multiple regression analysis, cord LDL-C remained the most significant association of cord adiponectin (beta = -0.13; P < 0.001). We did not find any significant ethnic differences in cord adiponectin or lipids with the exception of triglycerides, which were significantly lower in South Asian newborns (P < 0.05). CONCLUSION: This is the first report of an inverse relationship between cord adiponectin and LDL-C at birth. In contrast to adult studies, we found no significant association between adiponectin and HDL-C in cord blood. Our results and the strong independent association between adiponectin and HDL-C observed in adult studies suggest a role for adiponectin in lipid metabolism. Ethnic differences in adiponectin may arise after birth.