In the viewpoint of traditional Chinese medicine (TCM), the authors consider that simple obesity is not a disease, which does not fit to be treated according to the models of diagnosis and treatment in TCM. Considering its cause, pathogenesis, syndrome differentiation, principles and methods of treatment, as well as experimental study, etc. , the authors point out that the true effects of acupuncture on weight-loss should be investigated alone and avoid the influence of diet and exercise. Until now, what we have done on the acupuncture for treatment of simple obesity is not sufficient to verify the direct effects of acupuncture for weight-loss. The correct way for weight-loss is health care including dietary regime and regular life schedule. Comparatively, the treatment as the main choice for weight-loss is not recommended.
Acupuncture Therapy ; Animals ; Humans ; Obesity ; etiology ; physiopathology ; therapy ; Weight Loss

Adult ; Body Mass Index ; Child ; Humans ; Insulin Resistance ; Obesity ; complications ; Sleep Apnea, Obstructive ; etiology ; physiopathology

Animals ; Diet, Atherogenic ; Disease Models, Animal ; Heart ; physiopathology ; Myocardium ; pathology ; Obesity ; etiology ; physiopathology ; Rats ; Renin-Angiotensin System ; physiology

We investigated the change in activity of the sympathetic nervous system (SNS) in high-sucrose diet (HSD)-induced obese rats compared with controls. Power spectral analyses of R-R interval variability were performed to obtain the low frequency (LF, 0.04-0.699 Hz) and high frequency (HF, 0.7-3.0 Hz) powers. The percents of fat mass to body weight (%F/BW) and fat to muscle ratios (F/M) were significantly increased in HSD-fed rats. Plasma glucose, leptin, and triglyceride concentrations in rats fed with HSD were significantly increased. LF in normalized units (LFn), which represents both sympathetic and parasympathetic activities, was significantly increased whereas HF in normalized unit (HFn), which represents parasympathetic activity, was significantly decreased in HSD-fed rats. LF/HF, which represents sympathetic activity, was significantly increased in HSD-fed rats and was correlated with leptin (r=0.549, p<0.023), %F/BW (r=0.513, p<0.035), F/M (r=0.536, p<0.038), and triglyceride (r=0.497, p<0.042). When adjusted for leptin concentrations, however, LF/HF of HSD-fed rats was significantly decreased. In conclusion, HSD-induced obese rats showed increased LF/HF, which was significantly decreased by adjustment for leptin concentrations. We suggest that stimulating effect of leptin on SNS is reduced, which might play a role in induction of obesity by HSD.
Animal ; Body Weight ; Dietary Carbohydrates/administration & dosage ; Disease Models, Animal ; Fats/metabolism ; Male ; Muscles ; Obesity/physiopathology* ; Obesity/metabolism ; Obesity/etiology ; Rats ; Rats, Wistar ; Spectrum Analysis, Mass/methods ; Sympathetic Nervous System/physiopathology*

Obesity is a major cause of insulin resistance and type 2 diabetes. The altered glucose homeostasis is caused by faulty insulin signal transduction, which results in decreased glucose uptake by the muscle, altered lipogenesis, and increased glucose output by the liver. The etiology of this derangement in insulin signaling is related to a chronic inflammatory state, leading to the induction of inducible nitric oxide synthase and release of high levels of nitric oxide and reactive nitrogen species, which together cause posttranslational modifications in the signaling proteins. There are substantial differences in the molecular mechanisms of insulin resistance in muscle versus liver. Hormones and cytokines from adipocytes can enhance or inhibit both glycemic sensing and insulin signaling. The role of the central nervous system in glucose homeostasis also has been well established. Multi-pronged therapies aimed at rectifying obesity induced anomalies in both central nervous system and peripheral tissues may prove to be beneficial. The golden standard method to evaluate the insulin sensitivity is hyperinsulinemic euglycemic clamp.
Diabetes Mellitus, Type 2 ; etiology ; Glucose ; metabolism ; Humans ; Insulin ; metabolism ; Insulin Resistance ; physiology ; Obesity ; complications ; metabolism ; physiopathology

OBJECTIVEThe strong relation between type 2 diabetes mellitus and obesity with acanthosis nigricans is widely concerned. This study investigated the pancreatic beta-cell function in obese children with acanthosis nigricans, so as to find out the role of insulin secretion and insulin resistance in obese children with acanthosis nigricans.

METHODSThirty-five obese children with acanthosis nigricans (19 males and 16 females with mean age 12.8 +/- 1.5 years) were enrolled in this study. Thirty-eight obese children (21 boys and 17 girls with mean age 11.9 +/- 2.6 years) and 39 normal children (20 boys and 19 girls with mean age 11.2 +/- 2.2 years) were recruited as obese and normal control groups. The levels of serum fasting insulin, C-peptide, proinsulin and true insulin were measured in all the subjects. The ratios of proinsulin/insulin and proinsulin/C-peptide were calculated. Homeostasis model assessment was applied to assess the status of insulin resistance and basic function of pancreatic beta-cell.

RESULTSThe levels of fasting insulin, C-peptide proinsulin, true insulin, the ratios of proinsulin/insulin and proinsulin/C-peptide, insulin resistance index and insulin secretion index of obese children with acanthosis nigricans, obese control children and normal control children were: 18.5 (5.0-60.5) pmol/L, 12.4 (6.1-35.8) pmol/L and 5.1 (2.0-32.8) pmol/L; 3.9 (1.3-14.0) microg/L, 2.4 (1.1-4.0) microg/L and 1.1 (1.0-4.2) microg/L; 28.8 (9.9-64.2) pmol/L, 9.5 (2.2-34.5) pmol/L and 4.2 (2.0-16.0) pmol/L; 33.0 (6.2-66.0) pmol/L, 10.6 (4.8-29.4) pmol/L and 4.5 (1.3-30.1) pmol/L; 1.2 (0.4-8.9), 0.9 (0.2-1.9) and 0.8 (0.4-2.0); 6.9 (2.5-36.6), 4.7 (1.2-12.3) and 3.6 (1.2-9.6); 5.0 (0.8-14.1), 2.6 (1.3-8.1) and 1.2(0.4-6.9); 303.3 (52.2-1,163.8), 213.6 (84.6-572.0) and 51.1 (19.1-561.4). The levels of fasting insulin, C-peptide, proinsulin, true insulin, the ratios of proinsulin/insulin and proinsulin/C-peptide, insulin resistance index and insulin secretion index in obese children with acanthosis nigricans were significantly higher than those in obese children (P < 0.001) and normal children (P < 0.001).

CONCLUSIONObese children with acanthosis nigricans had higher insulin resistance and pancreatic beta-cell dysfunction; acanthosis nigricans may be a skin sign of high risk of type 2 diabetes mellitus.

Acanthosis Nigricans ; complications ; Adolescent ; C-Peptide ; blood ; Child ; Diabetes Mellitus, Type 2 ; etiology ; Female ; Humans ; Insulin ; blood ; Insulin Resistance ; Islets of Langerhans ; physiopathology ; Male ; Obesity ; complications ; physiopathology ; Proinsulin ; blood

AIMTo examine the changes in the erectile function in diet-induced obese rats and investigate the oral efficacy of DA-8159, a new phosphodiesterase type 5 (PDE5) inhibitor, on penile erection in obese rats.

METHODSThe rats were fed a high-energy diet for 12 weeks and divided into three groups: an obesity-resistant (OR) control group, an obesity-prone (OP) control group, and an OP-DA-8159 treatment (DA-8159) group. The electrostimulation-induced erectile responses were measured in all groups. The body weight, plasma cholesterol, triglyceride and glucose levels were also measured.

RESULTSIn the OP control group, the maximum intracavernous pressure (ICP) and ICP/blood pressure (ICP/BP) ratio after electric stimulation were significantly lower than those in OR control group. The corresponding area under the curve (AUC) of the ICP/BP ratio, the detumescence time and the baseline cavernous pressure were also lower than those in the OR control group, but this difference was not significant. The body weight gain, plasma cholesterol and triglyceride level in the OP group were significantly higher than those in the OR group. After administering the DA-8159, a significant increase in the maximum ICP and the ICP/BP ratio were observed. The corresponding AUCs in the DA-8159 group were also higher than those in the two control groups. Furthermore, the detumescence time was significantly prolonged after treatment with DA-8159.

CONCLUSIONThese results demonstrate that diet-induced obesity affects the erectile function in rats and these erectile dysfunction (ED) can be improved by the treatment with DA-8159, indicating DA-8159 might be a treatment option for ED associated with obesity.

Animal Feed ; Animals ; Diet ; Erectile Dysfunction ; etiology ; prevention & control ; Male ; Obesity ; etiology ; physiopathology ; Penile Erection ; drug effects ; physiology ; Phosphodiesterase Inhibitors ; pharmacology ; Pyrimidines ; pharmacology ; Rats ; Sulfonamides

PURPOSE: Obesity has been suggested to be linked to asthma. However, it is not yet known whether obesity directly leads to airway hyperreactivity (AHR) or obesity-induced airway inflammation associated with asthma. We investigated obesity-related changes in adipokines, AHR, and lung inflammation in a murine model of asthma and obesity. MATERIALS AND METHODS: We developed mouse models of chronic asthma via ovalbumin (OVA)-challenge and of obesity by feeding a high-fat diet, and then performed the methacholine bronchial provocation test, and real-time PCR for leptin, leptin receptor, adiponectin, adiponectin receptor (adipor1 and 2), vascular endothelial growth factor (VEGF), transforming growth factor (TGF) beta, and tumor necrosis factor (TNF) alpha in lung tissue. We also measured cell counts in bronchoalveolar lavage fluid. RESULTS: Both obese and lean mice chronically exposed to OVA developed eosinophilic lung inflammation and AHR to methacholine. However, obese mice without OVA challenge did not develop AHR or eosinophilic inflammation in lung tissue. In obese mice, lung mRNA expressions of leptin, leptin receptor, VEGF, TGF, and TNF were enhanced, and adipor1 and 2 expressions were decreased compared to mice in the control group. On the other hand, there were no differences between obese mice with or without OVA challenge. CONCLUSION: Diet-induced mild obesity may not augment AHR or eosinophilic lung inflammation in asthma.
Animals ; Asthma/physiopathology ; Bronchial Hyperreactivity/*physiopathology ; Bronchoalveolar Lavage Fluid/chemistry ; Dietary Fats/adverse effects ; Mice ; Obesity/*etiology/*physiopathology ; Pneumonia/*physiopathology ; Transforming Growth Factors/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Vascular Endothelial Growth Factor A/metabolism

Gastrointestinal (GI) motility has a crucial role in the food consumption, digestion and absorption, and also controls the appetite and satiety. In obese patients, various alterations of GI motility have been investigated. The prevalence of GERD and esophageal motor disorders in obese patients are higher than those of general population. Gastric emptying of solid food is generally accelerated and fasting gastric volume especially in distal stomach is larger in obese patients without change in accommodation. Contractile activity of small intestine in fasting period is more prominent, but orocecal transit is delayed. Autonomic dysfunction is frequently demonstrated in obese patients. These findings correspond with increased appetite and delayed satiety in obese patients, but causes or results have not been confirmed. Therapeutic interventions of these altered GI motility have been developed using botulinum toxin, gastric electrical stimulation in obese patients. Novel agents targeted for GI hormone modulation (such as ghrelin and leptin) need to be developed in the near future.
Botulinum Toxins/therapeutic use ; Colon/*physiopathology ; Eating ; Electric Stimulation Therapy ; Esophageal Motility Disorders/etiology/*physiopathology/therapy ; *Gastrointestinal Motility ; Ghrelin/therapeutic use ; Humans ; Intestine, Small/*physiopathology ; Leptin/therapeutic use ; Obesity/*complications ; Satiety Response ; Stomach/innervation/*physiopathology

PURPOSE: Reduced heart rate variability significantly increases cardiovascular mortality. Metabolic syndrome increases the cardiac autonomic dysfunction. Recently, increasing cardiovascular mortality has been reported in patients with schizophrenia. This study was done to compare heart rate variability between adults with and without schizophrenia and to compare the relationship of heart rate variability to metabolic syndrome in hospitalized patients with schizophrenia. METHODS: This was a descriptive and correlational study in which 719 adults without schizophrenia and 308 adults with schizophrenia took part between May and June 2008. We measured the following: five-minute heart rate variability; high-frequency, low-frequency, the ratio of low-frequency to high-frequency, and the Standard Deviation of all the normal RR intervals. Data was also collected on metabolic syndrome, abdominal obesity, triglycerides, HDL cholesterol, blood pressure and fasting glucose. RESULTS: The Standard Deviation of all the normal RR intervals values of heart rate variability indices were 1.53+/-0.18. The low-frequency and high-frequency values of heart rate variability indices were significantly higher in hospitalized patients with schizophrenia (3.89+/-1.36; 3.80+/-1.20) than those in the healthy participants (2.20+/-0.46; 2.10+/-0.46). There were no significant differences between the schizophrenic patients with and without metabolic syndrome. CONCLUSION: The results of this study indicate that schizophrenia patients have significantly lower cardiac autonomic control, but they have significantly higher low-frequency and high-frequency values than those of healthy adults. Use of antipsychotic drug may affect the autonomic nervous system in schizophrenic patients. Metabolic syndrome was not associated with cardiac autonomic control in schizophrenia patients.
Adult ; Autonomic Nervous System/physiopathology ; Blood Glucose/analysis ; Blood Pressure ; Cardiovascular Diseases/complications/diagnosis/mortality ; Cholesterol, HDL/blood ; Female ; *Heart Rate ; Hospitalization ; Humans ; Male ; Metabolic Syndrome X/*complications/*physiopathology ; Middle Aged ; Obesity/etiology ; Schizophrenia/*complications/mortality/*physiopathology ; Triglycerides/blood