Enterohormonal Changes After Digestive Adaptation: Five-Year Results of a Surgical Proposal to Treat Obesity and Associated Diseases

Santoro, Sérgio; Milleo, Fábio Quirilo; Malzoni, Carlos Eduardo; Klajner, Sidney; Borges, Pedro C. M.; Santo, Marco Aurélio; Campos, Fábio Guilherme; Artoni, Roberto Ferreira

doi:10.1007/s11695-007-9371-0

Cited by 73 publications

(56 citation statements)

References 35 publications

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“…Both DJB and jejunal resection normalized S I in diabetic rats as shown by S I levels equivalent to those of Wistar rats (S I = 1.01 6 0.06 3 10 24 min 21 $ pM 21 ; P = NS). Glucose effectiveness did not change after operations in any group.…”

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confidence: 76%

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Duodenal-Jejunal Bypass and Jejunectomy Improve Insulin Sensitivity in Goto-Kakizaki Diabetic Rats Without Changes in Incretins or Insulin Secretion

et al. 2014

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Gastric bypass surgery can dramatically improve type 2 diabetes. It has been hypothesized that by excluding duodenum and jejunum from nutrient transit, this procedure may reduce putative signals from the proximal intestine that negatively influence insulin sensitivity (SI). To test this hypothesis, resection or bypass of different intestinal segments were performed in diabetic Goto-Kakizaki and Wistar rats. Rats were randomly assigned to five groups: duodenal-jejunal bypass (DJB), jejunal resection (jejunectomy), ileal resection (ileectomy), pair-fed sham-operated, and nonoperated controls. Oral glucose tolerance test was performed within 2 weeks after surgery. Baseline and poststimulation levels of glucose, insulin, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) were measured. Minimal model analysis was used to assess SI. SI improved after DJB (SI = 1.14 ± 0.32 × 10(-4) min(-1) ⋅ pM(-1)) and jejunectomy (SI = 0.80 ± 0.14 × 10(-4) min(-1) ⋅ pM(-1)), but not after ileectomy or sham operation/pair feeding in diabetic rats. Both DJB and jejunal resection normalized SI in diabetic rats as shown by SI levels equivalent to those of Wistar rats (SI = 1.01 ± 0.06 × 10(-4) min(-1) ⋅ pM(-1); P = NS). Glucose effectiveness did not change after operations in any group. While ileectomy increased plasma GIP levels, no changes in GIP or GLP-1 were observed after DJB and jejunectomy. These findings support the hypothesis that anatomic alterations of the proximal small bowel may reduce factors associated with negative influence on SI, therefore contributing to the control of diabetes after gastric bypass surgery

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confidence: 76%

“…) and jejunectomy (S I = 0.80 6 0.14 3 10 24 min 21 $ pM 21 ), but not after ileectomy or sham operation/pair feeding in diabetic rats. Both DJB and jejunal resection normalized S I in diabetic rats as shown by S I levels equivalent to those of Wistar rats (S I = 1.01 6 0.06 3 10 24 min 21 $ pM 21 ; P = NS).…”

mentioning

confidence: 92%

Duodenal-Jejunal Bypass and Jejunectomy Improve Insulin Sensitivity in Goto-Kakizaki Diabetic Rats Without Changes in Incretins or Insulin Secretion

et al. 2014

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“…33 Finally, a recent report of 228 subjects who had sleeve gastrectomy, omentectomy and initial jejunectomy demonstrated increases in PYY and GLP-1 levels postprandially in a subgroup of 17 subjects, which was accompanied by earlier satiety, no adverse effects and better quality of life 5 years after surgery. 34 There are discrepancies regarding the potential role of PYY as a satiety factor. Peripheral injections of PYY 3-36 into rats inhibited food intake and reduced weight gain, whereas an infusion into humans reduced appetite and food intake, 4 as well as decreased caloric intake in obese and lean subjects.…”

Section: Discussionmentioning

confidence: 99%

Postprandial changes in gut regulatory peptides in gastric bypass patients

et al. 2008

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Objective: The marked weight loss induced by Roux-en-Y gastric bypass (RYGBP) for morbid obesity is still incompletely understood. It has been suggested that, besides the restriction imposed by the surgical procedure, alterations in gut regulatory peptides signaling the brain might contribute. The aim of this study was to measure the putative satiety peptides peptide YY (PYY), glucagon-like peptide-1 (GLP-1), pancreatic polypeptide (PP) and pro-neurotensin (pro-NT) in response to fasting and feeding. Design: The study is a cross-sectional study. After a prolonged overnight 14 h fast, a standardized mixed meal (574 kcal) was provided. Blood samples for peptide measurements were obtained before and after the meal. Subjects: Forty subjects (20 males and females) were included; 10 morbidly obese; (mean age 41 ± 7 years; mean BMI 44 ± 3 kg/m 2 ), 10 operated with RYGBP (age 45 ± 5 years; BMI 35 ± 6 kg/m 2 ), 10 aged-matched lean (age 44 ± 5 years; BMI 24 ± 3 kg/m 2 ) and 10 young lean subjects (age 26 ± 2 years; BMI 23 ± 2 kg/m 2 ). Measurements: Plasma concentrations of PYY, GLP-1, PP and pro-NT were obtained. Results: PYY levels increased more in the RYGBP group than in the other groups after the test meal. GLP-1 levels rose in the RYGBP patients, with a small increase seen in the age-matched lean group. PP concentrations increased similarly in all groups postprandially. Pro-NT levels were highest in surgical patients, with no meal effect. Conclusion: RYGBP subjects displayed exaggerated PYY and GLP-1 responses to a standardized meal and demonstrated higher pro-NT levels both pre-and postprandially. The findings indicate that possibly the alterations in gut peptide secretion may promote weight loss after gastric bypass surgery.

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“…Additionally, Pardina et al (2012) showed that gastric bypass leads to normalisation of the hematological profile and a decrease in PAI-1 levels which in turn results in a decreased risk of thromboembolism in severely obese individuals. Bariatric surgery has also been shown to maintain raised levels of adiponectin, an anti-inflammatory agent (Nijhuis et al, 2007) and resistin which may contribute to a decrease in atherosclerotic events post surgery (Santoro et al, 2008). Hence bariatric surgery may be an effective way of managing obesity and cardiac failure with subsequent knock on effects on the metabolic syndrome, coronary heart disease, and type II diabetes (Ashrafian, le Roux, Darzi, & Athanasiou, 2008) compared to other weight loss therapies.…”

Section: Effects Of Weight Loss On Fibrinolysismentioning

confidence: 99%

The Role of Plasminogen Activator Inhibitor-1 in the Metabolic Syndrome and Its Regulation

Phelan¹,

Kerins²

2014

JFR

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Obesity is a major risk factor for cardiovascular disease (CVD). Lipid abnormalities, hypertension, impaired glucose tolerance or diabetes, are cardiovascular risk factors that are frequently present in patients with obesity. Haemostatic and fibrinolytic disturbances are also considered to be important risk factors for CVD hence, a potential link between CVD, obesity and the metabolic syndrome arises. Regulation of the fibrinolytic system can occur at the level of plasminogen activators and plasminogen activator inhibitor-1 (PAI-1). PAI-1, a glycoprotein, is one of the most important inhibitors of fibrinolysis. Regulation of this serine protease inhibitor may have a beneficial effect on other conditions associated with the metabolic syndrome. Human adipose tissue is a source of PAI-1. PAI-1 production may in turn be controlled by a number of hormones and cytokines which are secreted by adipose tissue in addition to dietary factors. In this review we summarise the current knowledge regarding the role of altered fibrinolytic function in obesity, CVD and hence the metabolic syndrome. Regulatory factors including different dietary components, weight loss and dietary intervention will also be discussed.

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Enterohormonal Changes After Digestive Adaptation: Five-Year Results of a Surgical Proposal to Treat Obesity and Associated Diseases

Cited by 73 publications

References 35 publications

Duodenal-Jejunal Bypass and Jejunectomy Improve Insulin Sensitivity in Goto-Kakizaki Diabetic Rats Without Changes in Incretins or Insulin Secretion

Duodenal-Jejunal Bypass and Jejunectomy Improve Insulin Sensitivity in Goto-Kakizaki Diabetic Rats Without Changes in Incretins or Insulin Secretion

Postprandial changes in gut regulatory peptides in gastric bypass patients

The Role of Plasminogen Activator Inhibitor-1 in the Metabolic Syndrome and Its Regulation

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