scholarly journals Effects of Transoral Gastroplasty on Glucose Homeostasis in Obese Subjects

2013 ◽  
Vol 98 (5) ◽  
pp. 1901-1910 ◽  
Author(s):  
Laura Leccesi ◽  
Simona Panunzi ◽  
Andrea De Gaetano ◽  
Pietro Familiari ◽  
Amerigo Iaconelli ◽  
...  
2020 ◽  
Vol 45 (10) ◽  
pp. 1092-1098
Author(s):  
Soodabeh Aliashrafi ◽  
Mehrangiz Ebrahimi-Mameghani ◽  
Mohammad Asghari Jafarabadi ◽  
Lida Lotfi-Dizaji ◽  
Elnaz Vaghef-Mehrabany ◽  
...  

As there is limited and inconsistent evidence in potential role of vitamin D on insulin resistance and matrix metalloproteinases, this study aimed to examine the effect of vitamin D supplementation on glucose homeostasis, insulin resistance, and matrix metalloproteinases in obese subjects with vitamin D deficiency. A total of 44 participants with serum 25-hydroxyvitamin D (25(OH)D) level ≤ 50 nmol/L and body mass index (BMI) 30–40 kg/m2 were randomly allocated into receiving weight reduction diet with either 50 000 IU vitamin D3 pearl (n = 22) or placebo (n = 22) once weekly for 12 weeks. Primary outcomes were changes in fasting serum glucose (FSG), homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and matrix metalloproteinases (MMPs). Secondary outcomes were changes in weight, BMI, 25(OH)D, calcium, phosphorous and parathyroid hormone (PTH). Sun exposure and dietary intakes were also assessed. Serum levels of 25(OH)D3 increased significantly with a simultaneous decrease in serum concentration of PTH in the vitamin D group. Weight, BMI, FSG, and MMP-9 decreased significantly in both groups, and there were significant differences in changes in weight, serum 25(OH)D3, PTH, and MMP-9 levels between the groups. Within- and between-groups analysis revealed no significant differences in serum calcium, phosphorous, serum insulin, HOMA-IR, QUICKI, and MMP-2 after intervention. Our results indicated that improvement in vitamin D status resulted in greater reductions in weight and MMP-9 during weight loss. These preliminary results are sufficient to warrant a bigger study group.


2008 ◽  
Vol 247 (2) ◽  
pp. 270-275 ◽  
Author(s):  
Rosa Morínigo ◽  
Josep Vidal ◽  
Antonio M. Lacy ◽  
Salvadora Delgado ◽  
Roser Casamitjana ◽  
...  

2010 ◽  
Vol 20 (3) ◽  
pp. 202-207 ◽  
Author(s):  
C. Chiellini ◽  
A. Iaconelli ◽  
P. Familiari ◽  
M.E. Riccioni ◽  
M. Castagneto ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Akhila Mallipedhi ◽  
Sarah L. Prior ◽  
Gareth Dunseath ◽  
Richard M. Bracken ◽  
Jonathan Barry ◽  
...  

Aim. We examined endocannabinoids (ECs) in relation to bariatric surgery and the association between plasma ECs and markers of insulin resistance.Methods. A study of 20 participants undergoing bariatric surgery. Fasting and 2-hour plasma glucose, lipids, insulin, and C-peptide were recorded preoperatively and 6 months postoperatively with plasma ECs (AEA, 2-AG) and endocannabinoid-related lipids (PEA, OEA).Results. Gender-specific analysis showed differences in AEA, OEA, and PEA preoperatively with reductions in AEA and PEA in females postoperatively. Preoperatively, AEA was correlated with 2-hour glucose (r=0.55,P=0.01), HOMA-IR (r=0.61,P=0.009), and HOMA %S (r=-0.71,P=0.002). OEA was correlated with weight (r=0.49,P=0.03), waist circumference (r=0.52,P=0.02), fasting insulin (r=0.49,P=0.04), and HOMA-IR (r=0.48,P=0.05). PEA was correlated with fasting insulin (r=0.49,P=0.04). 2-AG had a negative correlation with fasting glucose (r=-0.59,P=0.04).Conclusion. Gender differences exist in circulating ECs in obese subjects. Females show changes in AEA and PEA after bariatric surgery. Specific correlations exist between different ECs and markers of obesity and insulin and glucose homeostasis.


2011 ◽  
Vol 96 (1) ◽  
pp. E146-E150 ◽  
Author(s):  
Takara L. Stanley ◽  
Markella V. Zanni ◽  
Stine Johnsen ◽  
Sarah Rasheed ◽  
Hideo Makimura ◽  
...  

Context and Objective: Obesity is associated with activation of the TNF-α system, increased inflammatory markers, and insulin resistance. Although studies in rodents suggest that attenuation of TNF activity improves glucose homeostasis, the effect of prolonged inhibition of TNF-α with etanercept on inflammation and glucose homeostasis in a human model of obesity is not known. Design and Participants: Forty obese subjects with features of metabolic syndrome were randomized to etanercept or placebo, 50 mg twice weekly for 3 months, followed by 50 mg once weekly for 3 months. Outcome Measures: Subjects underwent oral glucose tolerance testing and measurement of serum inflammatory biomarkers and adipokines. Subcutaneous fat biopsy was performed in a subset for measurement of adipokine and TNF-α mRNA expression. Results: Visceral adiposity was significantly associated with serum concentrations of TNF receptor 1 (TNFR1), TNFR2, and vascular cell adhesion molecule-1 and adipose tissue expression of TNF-α and SOCS-3 (all P < 0.05). Insulin resistance as assessed by homeostasis model assessment was significantly associated with TNFR1, C-reactive protein, IL-6, and soluble intracellular adhesion molecule-1 (sICAM-1) (all P < 0.05). Etanercept significantly improved fasting glucose (treatment effect vs. placebo over 6 months, −10.8 ± 4.4%, P = 0.02). Etanercept also increased the ratio of high molecular weight adiponectin to total adiponectin (+22.1 ± 9.2% vs. placebo, P = 0.02), and decreased levels of sICAM-1 (−11 ± 2% vs. placebo, P < 0.0001). In contrast, body composition, lipids, C-reactive protein, and IL-6 were unchanged after 6 months. Conclusions: Prolonged therapy with etanercept improved fasting glucose, increased the ratio of high molecular weight to total adiponectin, and decreased sICAM-1 in obese subjects with abnormal glucose homeostasis and significant subclinical inflammation.


2014 ◽  
Vol 99 (6) ◽  
pp. 2155-2163 ◽  
Author(s):  
Heli Viljakainen ◽  
Kaisa K. Ivaska ◽  
Päivi Paldánius ◽  
Marita Lipsanen-Nyman ◽  
Tero Saukkonen ◽  
...  

Context: Observations in rodents suggest that osteocalcin (OC) participates in glucose metabolism. Based on human studies, it remains unclear whether circulating OC is simply a bone turnover marker (BTM) or also a mediator in interactions between the skeleton and glucose homeostasis. Objective: The objective of the study was to determine the responses of BTMs, including OC, to oral glucose tolerance test (OGTT) in a case-control setting. Design and Patients: Thirty-four normoglycemic young adults [mean age 19 y (SD 2.3)] with severe childhood-onset obesity and their gender- and age-matched nonobese controls underwent a standard 2-hour OGTT. Main Outcome Measures: Glucose, insulin, and six BTMs including total and carboxylated OC (cOC) were determined at baseline and at 30, 60, 90, and 120 minutes during OGTT. Results: The obese and control subjects were similar in height; the mean body mass indices were 40.4 and 21.9 kg/m2, respectively. The homeostasis model assessment index was 2.7 times greater in the obese subjects. All BTMs, except bone-specific alkaline phophatase, were lower in the obese subjects compared with the controls: the differences at baseline were 40%, 35%, 17%, 31%, and 32% for N-terminal propeptides of type I collagen, cross-linked telopeptides of type I collagen, tartrate-resistant acid phosphatase, total OC, and carboxylated OC (P < .05 for all) after adjusting for whole-body bone area. All BTMs decreased during OGTT. The relative values for the OGTT responses for total, but not for cOC (measured as area under the curve) differed between the two groups (P = .029 and P = .139, respectively): the decrease in total OC during the OGTT was less pronounced in the obese subjects. Responses in other BTMs were similar between the groups. No associations were observed between glucose metabolism and OCs during OGTT with linear regression. Conclusions: Bone turnover markers were substantially lower in obese subjects compared with controls. Total OC and cOC showed less pronounced decrease during the OGTT in obese subjects compared with controls, whereas other BTMs responded similarly in the two groups. The role of OC, if anything, in glucose homeostasis is indirect and may be mediated via other factors than glucose or insulin.


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