Gastric Plication and Sleeve Gastrectomy in an Experimental Model of Obesity: New Insights into Weight Loss, Intake and Metabolic Results.

AIM: Laparoscopic gastric plication (LGP) is a bariatric surgical technique based on the anatomical principles of laparoscopic sleeve gastrectomy (LSG), but its effects on the metabolic profile are still uncertain. The aim of our study is to compare the changes in weight, metabolic parameters and gastric histology following intervention by gastric plication (GP) and sleeve gastrectomy (SG) in an experimental model of obesity. METHODS: To conduct the study, 32 8-week-old male Sprague-Dawley rats (Charles River®) were fattened by means of a cafeteria diet and randomly assigned to the following experimental groups: group 1: GP (n = 12); group 2: SG (n = 12) and group 3: sham (n = 8). RESULTS: Unlike the SG group, the GP group attained the weight of the sham group at the end of the experiment (week 16). The GP group continued to eat more cafeteria diet than the SG group. In addition, the SG group achieved better glycaemic control than the GP group. Significantly higher plasma ghrelin levels were observed at week 16 in the GP group than in the SG group (2.29 ± 0.5 vs 1.07 ± 0.4, p < 0.05), which also occurred for the glucagon plasmatic levels (62.71 ± 36.2 vs 24.63 ± 9.3, p < 0.05). CONCLUSIONS: GP is not as effective as SG and cannot be considered a metabolic surgery due to observed hormonal variations. The animals subjected to a GP continued to have a high appetite for the cafeteria diet unlike the animals submitted to an SG. Hormonal mechanisms possibly related to glucagon and ghrelin may be involved in this metabolic response.

Analysis of Gastric Physiology After Laparoscopic Sleeve Gastrectomy (LSG) With or Without Antral Preservation in Relation to Metabolic Response: a Randomised Study.

INTRODUCTION: Laparoscopic sleeve gastrectomy is one of the most common techniques in bariatric surgery, but there is no consensus on the optimal distance from the pylorus to start the gastric transection. The aim of this study is to determine the differences in gastric emptying, gastric distension and metabolic response between two starting distances. MATERIAL AND METHODS: This is a prospective randomised study of 60 patients (30 patients with the section at 3 cm and 30 patients at 8 cm from the pylorus). We calculate at 6 and 12 months from surgery gastric emptying by scintigraphy (T1/2 min), gastric volume by CT scan (cc) and metabolic response by blood sample analysis (glucose, HbA1c, insulin, HOMA-IR, GLP-1, GIP and C-peptide). RESULTS: Gastric emptying increases the speed significantly in both groups but is greater in the 3-cm group (p < 0.05). Dividing groups into type 2 diabetic patients and non-diabetic patients, the speed in non-diabetic patients is significantly higher for the 3-cm group. Residual volume increases significantly in both groups, and there are no differences between them. One year after surgery, there are significant improvements in the hyperinsulinaemia in the patients of the 3-cm group with respect to the 8-cm group, but only in diabetic patients. No differences between groups are found regarding changes in GLP-1 or GIP. CONCLUSIONS: Gastric emptying is faster in patients with antrum resection. The distance does not influence the gastric emptying of diabetic patients. Other mechanisms may explain metabolic response besides GLP-1 and its association with improvements in diabetes via gastric emptying.

Mapping of the circulating metabolome reveals α-ketoglutarate as a predictor of morbid obesity-associated non-alcoholic fatty liver disease.

BACKGROUND: Obesity severely affects human health, and the accompanying non-alcoholic fatty liver disease (NAFLD) is associated with high morbidity and mortality. Rapid and non-invasive methods to detect this condition may substantially improve clinical care. METHODS: We used liquid and gas chromatography-quadruple time-of-flight-mass spectrometry (LC/GC-QTOF-MS) analysis in a non-targeted metabolomics approach on the plasma from morbidly obese patients undergoing bariatric surgery to gain a comprehensive measure of metabolite levels. On the basis of these findings, we developed a method (GC-QTOF-MS) for the accurate quantification of plasma α-ketoglutarate to explore its potential as a novel biomarker for the detection of NAFLD. RESULTS: Plasma biochemical differences were observed between patients with and without NAFLD indicating that the accumulation of lipids in hepatocytes decreased ß-oxidation energy production, reduced liver function and altered glucose metabolism. The results obtained from the plasma analysis suggest pathophysiological insights that link lipid and glucose disturbances with α-ketoglutarate. Plasma α-ketoglutarate levels are significantly increased in obese patients compared with lean controls. Among obese patients, the measurement of this metabolite differentiates between those with or without NAFLD. Data from the liver were consistent with data from plasma. Clinical utility was assessed, and the results revealed that plasma α-ketoglutarate is a fair-to-good biomarker in patients (n=230). Other common laboratory liver tests used in routine application did not favourably compare. CONCLUSION: Plasma α-ketoglutarate is superior to common liver function tests in obese patients as a surrogate biomarker of NAFLD. The measurement of this biomarker may potentiate the search for a therapeutic approach, may decrease the need for liver biopsy and may be useful in the assessment of disease progression.

Liver lipocalin 2 expression in severely obese women with non alcoholic fatty liver disease.

BACKGROUND: Lipocalin 2 (LCN2) has been related to obesity, insulin resistance and metabolic disturbance. However, its relation with non alcoholic fatty liver disease (NAFLD) has hardly been studied. METHODS: We examined LCN2 circulating levels and its protein and gene expression in liver from women with severe obesity and NAFLD. We analyzed the liver histology of 59 white severely obese women (BMI ≥40 Kg/m²): 15 subjects presented normal liver histology or non-significant liver disease (NL), 18 simple steatosis (SS) and 26 non alcoholic steatohepatitis (NASH). We determined the anthropometric and metabolic features of the women. LCN2 levels were determined by an ELISA and liver mRNA expression by real time RT-PCR. We also studied LCN2 expression in HepG2 liver cells under various inflammatory stimuli. RESULTS: Liver LCN2 protein and gene expression were higher in NAFLD than in obese with NL. Liver LCN2 gene expression correlated with SS (r=0.351, p=0.016), and its protein expression correlated with NASH (r=0.705, p=0.003). LCN2 expression was detected in HepG2 cells after the administration of TNFα, IL6, resistin or adiponectin. LCN2 expression was induced by TNFα, IL6 and resistin. CONCLUSIONS: Liver LCN2 is related to NAFLD in severely obese women. Up-regulation of LCN2 expression is detected in HepG2 cells after exposure to TNFα, IL6 and resistin. These results suggest that LCN2 expression is induced under liver harmful conditions.