scholarly journals Plasma Leptin Concentrations and Esophageal Hypomotility in Obese Patients

2015 ◽  
Vol 29 (1) ◽  
pp. 49-51 ◽  
Author(s):  
Justin Côté-Daigneault ◽  
Pierre Poitras ◽  
Rémi Rabasa-Lhoret ◽  
Mickael Bouin

BACKGROUND: Although esophageal hypomotility is prevalent in obese patients, its cause remains unknown. Leptin, a hormone derived from adipose tissue, may be involved in this phenomenon because it has been shown to decrease gastric and intestinal motility in animals. It has been hypothesized that elevated plasma leptin concentration is a risk factor for esophageal dysmotility in obese patients.OBJECTIVE: To determine whether plasma leptin concentrations are higher in obese patients with esophageal hypomotility than in obese patients with a normal motility profile.METHOD: Fasting plasma leptin concentration (assessed by radioimmuoassay) was measured in all patients who were included in a study protocol investigating esophageal manometry before bariatric surgery. The patients completed standardized surveys regarding epidemiological data, upper gastrointestinal symptoms, medical history and medication(s). Basal levels of leptin, as well as corrected leptin scores adjusted for sex and body mass index, were compared in patients with and without esophageal dysmotility.RESULTS: Nine patients without dysmotility and eight with dysmotility were included. Both groups were comparable with regard to age (42±9 versus 38±9 years), sex (78% versus 75% women) and body mass index (49±10 kg/m2versus 42±7 kg/m2). There were no significant differences regarding medication(s) and comorbidities between the two groups. When compared with normal predicted values, the corrected leptin scores were 30% higher in patients with dysmotility than in the control group with normal motility (P≤0.05).CONCLUSION: Obese patients with esophageal dysmotility exhibited elevated plasma leptin concentrations, suggesting a role for leptin in promoting esophageal hypomotility.

Author(s):  
Asmaa Reda Elsayed Elshazly ◽  
Mohammad Abdelhakeem Seleem ◽  
Mohamed Hamdy Abo-Ryia ◽  
Adel Abdel-Kareem Badawy

Background: Obesity is becoming an important issue for health promotion. The World Health Organization estimated that around 1.5 billion adults were overweight (body mass index (BMI) 25 kg/m2) and about 500 million people were obese (BMI 30 kg/m2) in 2008. The relationship between obesity and mental health is also considered important. In a community-based study, obesity was positively associated with several mental disorders, especially mood disorders and anxiety disorders. The aim of the study is the assessment of current and lifetime psychiatric disorders among morbidly obese patients. Methods: This case control study was conducted on 60 participants from outpatient clinic of GIT surgery unit and community. All participants were subjected to: Body weight and body mass index, Psychiatric interview for diagnosis of psychiatric disorders by Arabic version of MINI, Scale for diagnosis of Bulimia nervosa by Shokeer, Scale for diagnosis of Anorexia Nervosa by Shokeer, Binge Eating Disorder Screener-7, Eating attitude test, Hamilton Depressions Rating Scale and Hamilton anxiety scale. Results: There was a significant increase in anxiety in patients with morbid obesity compared to control group. There was a significant difference between both groups showing the high prevalence of depression in patients with morbid obesity. Based on EAT test, there was a significant prevalence of abnormal eating behaviors in patients group compared to none of control group. A screening test for the presence of Binge eating symptoms revealed significant increase of symptoms in patients’ group. Conclusions: Psychiatric disorders are prevalent in morbidly obese patients and are associated with significantly worse quality of life. In addition, morbidly obese patients had significantly worse physical and mental health relative to control group from general population. High rates of psychiatric disorders among morbidly obese patients seem to be the rule rather than an exception.


2009 ◽  
Vol 94 (11) ◽  
pp. 4499-4507 ◽  
Author(s):  
David M. Selva ◽  
Albert Lecube ◽  
Cristina Hernández ◽  
Juan A. Baena ◽  
José M. Fort ◽  
...  

Context: Zinc-α2 glycoprotein (ZAG) has been proposed as a new candidate in the pathogenesis of obesity, but most of the information stems from studies performed in rodents and in vitro assays. Objective: The main aim of the study was to compare serum levels of ZAG and its expression (mRNA levels and protein) in adipose tissue and the liver between obese and nonobese subjects. The relationship between ZAG and insulin resistance was also explored. Design: This was a case-control study. Setting: The study was conducted at a university referral center. Patients and Methods: Samples of serum, sc adipose tissue (SAT), visceral adipose tissue (VAT), and liver were obtained from 20 obese subjects during bariatric surgery. Samples from 10 nonobese patients matched by age and gender were used as a control group. Serum ZAG levels were determined by ELISA. ZAG mRNA levels were measured by real-time PCR and protein content by Western blot. The effect of insulin on liver production of ZAG was assessed using HepG2 cultures. Results: Serum concentration of ZAG (micrograms per milliliter) was significantly lower in obese subjects (40.87 ± 10.45 vs. 63.26 ± 16.40; P = 0.002). ZAG expression was significantly lower in the adipose tissue (SAT and VAT) and liver of obese patients than in control subjects. Significant negative correlations between body mass index and circulating ZAG (r = −0.65, P < 0.001) as well as between body mass index and mRNA ZAG levels in SAT (r = −0.68, P < 0.001) and VAT were detected (r = −0.64, P < 0.001). No relationship was found between ZAG and homeostasis model assessment for insulin resistance and insulin had no effect on ZAG production in vitro. Conclusion: A down-regulation of ZAG in SAT, VAT, and liver exists in obese patients but seems unrelated to insulin resistance. A downregulation of zinc-α2 glycoprotein in adipose tissue and liver exists in obese patients, and it is unrelated to insulin resistance.


2017 ◽  
Vol 11 (1) ◽  
pp. 54-60
Author(s):  
Suhad A. Mustafa

There have been numerous genetic causes of obesity specifically leptin, genetic variants of the leptin receptor gene (LEPR Gln223Arg) which appeared to be polymorphismized (A>G; rs1137101) have been implicated in the pathogenesis of obesity in several populations, although no association has been evidenced in other regions in the world. In this study, the association between LEPR Gln223Arg polymorphism with Body Mass Index (BMI) and plasma leptin levels in obese diabetic and obese non-diabetic adults who are randomly selected from Erbil city is evaluated. Blood samples were collected for DNA extraction, and plasma leptin measurements. LEPR (A > G; rs1137101) genotypes were identified by a PCR- RFLP. The results show that plasma leptin concentrations increased with body mass index, and in obese diabetic group was more than  two-fold increases p=0.001 when compared to those of obese non-diabetic patients. LEPR (A > G; rs1137101) gene polymorphisms did not found associated with BMI in the whole studied population. Furthermore an increased frequency of the GG genotype in the female control group 32.1 compared to obese group 19.2, but the frequency did not significant (OR= 1.38: 95% CI; 0.74-2.03, P=0.07 ) which indicated that this genotype might be associated with a protective effect against obesity in female only and that this effect was independent of diabetes. Further analysis of a larger population is required to confirm the biological relevance of this polymorphism for obesity in the Kurdish population.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Z. M. Patel ◽  
J. M. DelGaudio ◽  
S. K. Wise

Background. Morbidly obese patients demonstrate altered olfactory acuity. There has been no study directly assessing Body Mass Index (BMI) in patients with olfactory dysfunction. Our purpose was to compare BMI in a group of patients with subjective olfactory dysfunction to those without subjective olfactory complaints.Methods. Retrospective matched case-control study. Sixty patients who presented to a tertiary care otolaryngology center with subjective smell dysfunction over one year were identified. Neoplastic and obstructive etiologies were excluded. Demographics, BMI, and smoking status were reviewed. Sixty age, gender, and race matched control patients were selected for comparison. Chi-square testing was used.Results. 48 out of 60 patients (80%) in the olfactory dysfunction group fell into the overweight or obese categories, compared to 36 out of 60 patients (60%) in the control group. There was a statistically significant difference between the olfactory dysfunction and control groups for this stratified BMI(p= 0.0168).  Conclusion. This study suggests high BMI is associated with olfactory dysfunction. Prospective clinical research should examine this further to determine if increasing BMI may be a risk factor in olfactory loss and to elucidate what role olfactory loss may play in diet and feeding habits of obese patients.


Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 430 ◽  
Author(s):  
Daria Skuratovskaia ◽  
Larisa Litvinova ◽  
Maria Vulf ◽  
Pavel Zatolokin ◽  
Konstantin Popadin ◽  
...  

Mitochondrial DNA (mtDNA) encodes core subunits of oxidative phosphorylation complexes and, as a result of intricate regulatory crosstalk between nuclear and mitochondrial genomes, the total number of mtDNA copies fits the requirements of each cell type. Deviations from the physiological number of mtDNA copies are expected to be deleterious and might cause some inherited diseases and normal ageing. We studied 46 obese patients with type 2 diabetes (T2DM) one year after a laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (RYGB). The results were compared with normal-weight patients without T2DM (control group 1) (body mass index (BMI) = 22.5 ± 3.01 kg/m2) and patients with obesity without T2DM (control group 2) (BMI = 36 ± 3.45 kg/m2). We detected an increase of mtDNA copy number in the cells of the buffy coat obtained from peripheral blood, sampled one year after bariatric surgery. We also found that average mtDNA copy number as well as its dynamics (before and after the surgery) are gender-specific. To the best of our knowledge, this is the first evidence for the restoration of mtDNA copy number in obese patients after LSG and RYGB.


1999 ◽  
Vol 84 (12) ◽  
pp. 4545-4548 ◽  
Author(s):  
Eba H. Hathout ◽  
Jeannine Sharkey ◽  
Michael Racine ◽  
David Ahn ◽  
John W. Mace ◽  
...  

To test the hypothesis that insulin regulates leptin, we measured the plasma leptin concentration before and during treatment of diabetic ketoacidosis (DKA), a condition characterized by extreme insulin deficiency. The study included 17 patients with type 1 diabetes (7 males and 10 females), aged 10 ± 1 yr (mean ± se), with a body mass index of 17.6 ± 1.9 kg/m2. Patients were treated with continuous insulin infusion and fluid and electrolyte replacement. Plasma leptin was measured every 6 h in the first 24 h, during which patients received a total insulin dose of 0.6–2.0 U/kg. Plasma leptin concentrations were also measured in a control group of 29 stable type 1 diabetic children (12 males and 17 females) and 25 healthy children (11 males and 14 females), aged 11 ± 1 yr, with a body mass index of 18.5 ± 1.1 kg/m2. Before treatment, plasma leptin concentrations were significantly lower in patients with DKA than those in diabetic and healthy controls (4.9± 1.2 vs. 9.0 ± 1.8 and 11.2 ± 2.1 ng/mL, respectively; P < 0.05). In the DKA patients, plasma leptin increased to 6.4 ± 1.5, 7.5 ± 1.9, 9.1± 2.7, and 8.9 ± 2.5 at 6, 12, 18, and 24 h, respectively, after starting treatment (P = 0.001). Thus, leptin levels increased by 38 ± 10% and 92 ± 38% within 6 and 24 h of starting treatment. There was no difference in the change in plasma leptin by 24 h between subjects who could eat (n = 7) and those who could not (n = 10). The plasma leptin increase was paralleled by a rise in insulin level and a decline in glucose and cortisol levels at 6 and 24 h. In conclusion, DKA was associated with decreased plasma leptin concentrations. Treatment resulted in a significant increase in plasma leptin, which may be due to the effect of insulin on leptin production. Our data lend support to the hypothesis that insulin is the link between caloric intake and plasma leptin.


Medicina ◽  
2019 ◽  
Vol 55 (6) ◽  
pp. 228 ◽  
Author(s):  
Fatih Temiz ◽  
Hatice Güneş ◽  
Hakan Güneş

Background and Objective: Childhood obesity is one of the worldwide health problems with an increasing prevalence and accompanied by severe morbidity and mortality. It is a serious predisposing risk factor especially for the development of cardiovascular diseases and arrhythmias. Electromechanical delay (EMD) is known to be a predictor for the development of atrial fibrillation (AF). Our study aims to investigate whether EMD, which is a predictor of AF, prolongs in obese children or not. Material and Methods: The study included 59 obese patients aged between 8–18 years and 38 healthy patients as the control group with a similar age and gender. All the individuals underwent transthoracic echo and tissue Doppler echocardiography. Systolic and diastolic left ventricular (LV) functions, inter- and intra-atrial electromechanical delay were measured by tissue Doppler imaging (TDI) and conventional echocardiography. Results: Obese patients had significantly lengthened P-wave on surface ECG to the beginning of the late diastolic wave (PA) lateral, PA septum, intra- and inter-atrial electromechanical delays when compared with the control group (p < 0.001, p = 0.001, p < 0.001 and p < 0.001, respectively) Inter-atrial EMD and intra-atrial EMD correlated positively with body mass index (BMI) values (r = 0.484, p < 0.001 and r = 0.376, p = 0.001; respectively) BMI was significantly related with inter-atrial EMD (β = 0.473, p < 0.001) However, there was no relationship between inter-atrial EMD and serum glucose and platelet count. Conclusion: In our study, we declared that electromechanical delay was increased in obese children when compared to the control group and intra- and inter-atrial electromechanical delay was in correlation with body mass index. Furthermore, we discovered that BMI is an independent predictor of the inter-atrial EMD in obese children.


2009 ◽  
Vol 40 (3) ◽  
pp. 186-190 ◽  
Author(s):  
Samir Ben Ali ◽  
Amani Kallel ◽  
Yousra Sediri ◽  
Bouchra Ftouhi ◽  
Moncef Feki ◽  
...  

2013 ◽  
Vol 32 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Emina Čolak ◽  
Dragana Pap ◽  
Nada Majkić-Singh ◽  
Ivana Obradović

Summary Background: It has been reported that obesity is associated with metabolic syndrome, insulin resistance, cardiovascular risk but also with nonalcoholic fatty liver disease (NAFLD). The prevalence of obesity in children and adolescents is increasing rapidly all over the world. The aim of this study was to analyze the value of liver enzymes: AST, ALT and γGT in a group of obese students in order to establish their correlation to anthropometric parameters such as: BMI (body mass index), WC (waist circumference), HC (hip circumference), and WHR (waist-to-hip ratio) compared to non-obese students who comprised the control group (CG). Methods: In this study, 238 students from the University of Novi Sad of both sexes (126 men and 112 women) with a mean age of 22.32 ± 1.85 years were included. According to the body mass index (BMI) lower and higher than 25 kg/m2 and waist circumference (WC) lower and higher than 94 cm (80 cm for females) the whole group of 238 students was divided into 2 subgroups: the obese group at increased risk for CVD (Group 1) and the group at lower risk for CVD (Group 2). AST, ALT and γGT activities were determined in fasting blood samples. Results: Statistical processing data revealed significantly higher values of AST, ALT and γGT in the group of students with BMI>25 kg/m2, WC>94 cm for males and WC>80 cm for females, HC>108 cm for males and HC>111 cm for females, and WHR>0.90 for males and WHR>0.80 for females (P<0.001). Significant association was established between anthropometric parameters and liver enzyme levels (P<0.0001). Conclusions: Obese students with higher BMI, WC, HC and WHR values have higher liver enzyme activites and a higher chance to develop NAFLD in the future.


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