| 1. |
- Abdelhafez, A. H. K., et al.
(författare)
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Impact of Abdominal Subcutaneous Fat Reduction on Glycemic Control in Obese Patients with Type 2 Diabetes Mellitus
- 2018
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Ingår i: Bariatric Surgical Practice and Patient Care. - : Mary Ann Liebert Inc. - 2168-023X .- 2168-0248. ; 13:1, s. 25-32
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Tidskriftsartikel (refereegranskat)abstract
- Background: The effect on type 2 diabetes mellitus (T2DM) when adipose tissue is removed is controversial. This study aimed to evaluate and compare the effect of the abdominoplasty and bariatric surgery on glycemic control in patients with T2DM. Methods: Patients with T2DM undergoing abdominoplasty for cosmesis were studied (n=25). Subjects were 36.91.3 years with a preoperative body mass index (BMI) of 40.60.5kg/m(2) and mean glycated hemoglobin (HbA1c) of 7.4%+/- 0.2%. Fifteen matched patients undergoing bariatric surgery were selected as a comparator group. Weight, BMI, waist circumference (WC), random blood glucose (RBG), and HbA1c were evaluated at baseline and 3, 6, and 12 months postsurgery. Results: By 12 months, abdominoplasty reduced weight by 5.6 +/- 0.3kg p<0.01), and HbA1c was reduced to 6.8%+/- 0.3% (p<0.01). After 12 months, bariatric surgery reduced BMI from 42.2 +/- 1kg/m(2) to 26.6 +/- 0.4kg/m(2) (p<0.01). HbA1c reduced from 7.9%+/- 0.4% to 5.5%+/- 0.2% (p<0.01). WC was similar between both groups at 3 months, although HbA1c reductions were superior after bariatric surgery. Conclusions: Reducing subcutaneous adipose tissue with abdominoplasty results in a small improvement in glycemic control in patients with T2DM. Despite equivalent WC at 3 months, bariatric surgery outperformed abdominoplasty on all metabolic parameters then and thereafter.
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| 2. |
- Al-Najim, Werd, et al.
(författare)
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Food intake and eating behavior after bariatric surgery
- 2018
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Ingår i: Physiological Reviews. - : American Physiological Society. - 0031-9333 .- 1522-1210. ; 98:3, s. 1113-1141
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Tidskriftsartikel (refereegranskat)abstract
- Obesity is an escalating global chronic disease. Bariatric surgery is a very efficacious treatment for obesity and its comorbidities. Alterations to gastrointestinal anatomy during bariatric surgery result in neurological and physiological changes affecting hypothalamic signaling, gut hormones, bile acids, and gut microbiota, which coalesce to exert a profound influence on eating behavior. A thorough understanding of the mechanisms underlying eating behavior is essential in the management of patients after bariatric surgery. Studies investigating candidate mechanisms have expanded dramatically in the last decade. Herein we review the proposed mechanisms governing changes in eating behavior, food intake, and body weight after bariatric surgery. Additive or synergistic effects of both conditioned and unconditioned factors likely account for the complete picture of changes in eating behavior. Considered application of strategies designed to support the underlying principles governing changes in eating behavior holds promise as a means of optimizing responses to surgery and long-term outcomes. © 2018 American Physiological Society. All rights reserved.
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| 3. |
- Al-Najim, W., et al.
(författare)
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Integrated insights into the role of alpha-melanocyte stimulatory hormone in the control of food intake and glycaemia
- 2018
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Ingår i: Peptides. - : Elsevier BV. - 0196-9781. ; 100, s. 243-248
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Tidskriftsartikel (refereegranskat)abstract
- Identifying peptide hormones with multipotent actions on both weight and glycaemia can have a significant impact on therapeutic options in the treatment of obesity and diabetes. This has been exemplified by recent advances involving pharmacological exploitation of glucagon-like peptide 1 biology. Herein, we summarise evidence supporting the potential candidacy in this light of alpha-melanocyte stimulatory hormone, an endogenous peptide hormone and a breakdown product of the neuropeptide pro-opiomelanocortin. We reference its well described central actions in the control of food intake and moreover highlight new data pointing to an important role for this peptide hormone in the periphery, in relation to glycaemic control.
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| 4. |
- Doody, A., et al.
(författare)
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Validating the association between plasma tumour necrosis factor receptor 1 levels and the presence of renal injury and functional decline in patients with Type 2 diabetes
- 2018
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Ingår i: Journal of Diabetes and Its Complications. - : Elsevier BV. - 1056-8727. ; 32:1, s. 95-99
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Elevated plasma soluble tumour necrosis factor receptor 1 (TNFR1) predicts long-term progression of chronic kidney disease. We investigated the association between elevated TNFR1 and the presence of renal disease in patients with Type 2 diabetes mellitus registering a haemoglobin Mc (HbA1c) >48 mmol/mol despite medical therapy. Methods: Using sensitivity, specificity and regression analyses we interrogated the association between plasma TNFR1 and presence of chronic kidney disease as assessed by the presence of microalbuminuria and/or an estimated glomerular filtration rate of less than 60 ml/min/1.73 m(2) (stages 3-5 chronic kidney disease). The association of TNFR1 with C-reactive protein and leptin-adiponectin ratio as plasma markers of systemic inflammation and adipose stress respectively was also investigated. Results: Upper quartile TNFR1 is independently associated with elevated urinary albumin-creatinine ratios, reductions in eGFR and strongly predicts the presence of stages 3-5 chronic kidney disease in regression modelling. Elevated TNFR1 levels are associated with increased plasma C-reactive protein and augmented leptin-adiponectin ratio. Conclusions: Our study confirms plasma TNFR1 as a surrogate of renal structural and functional impairment in patients with type 2 diabetes mellitus. Association of TNFR1 with markers of systemic inflammation and adipose stress indicates that TNFR1 may be a biomarker of these processes as components of the pathogenesis of diabetic kidney disease. (C) 2017 Elsevier Inc. All rights reserved.
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| 5. |
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| 6. |
- Sinclair, P., et al.
(författare)
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Metabolic Effects of Bariatric Surgery
- 2018
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Ingår i: Clinical Chemistry. - : Oxford University Press (OUP). - 0009-9147 .- 1530-8561. ; 64:1, s. 72-81
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Obesity can be defined as a chronic subcortical brain disease, as there is an important neurophysiological component to its etiology based on changes in the functioning of those areas of the brain controlling food intake and reward. Extensive metabolic changes accompany bariatric surgery-based treatment of obesity. Consequently, the term "metabolic" surgery is being increasingly adopted in relation to the beneficial effects these procedures have on chronic diseases like type 2 diabetes. CONTENT: In the present review, we focus on the key biochemical and physiological changes induced by metabolic surgery and highlight the beneficial effects accrued systemically with the use of an organ-based approach. Understanding the impact on and interactions between the gut, brain, adipose tissue, liver, muscle, pancreas, and kidney is key to understanding the sum of the metabolic effects of these operations. SUMMARY: Further mechanistic studies are essential to assess the true potential of metabolic surgery to treat metabolic comorbidities of obesity beyond type 2 diabetes. Approaches that may mitigate the metabolic side effects of surgery also require attention. Understanding the positive impact of metabolic surgery on metabolic health may result in a wider acceptance of this intervention as treatment for metabolic, comorbid conditions.
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| 7. |
- Werling, Malin, 1967, et al.
(författare)
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Biliopancreatic Diversion is associated with greater increases in energy expenditure than Roux-en-Y Gastric Bypass
- 2018
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Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 13:4
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Tidskriftsartikel (refereegranskat)abstract
- Objective The greater weight loss achieved following Biliopancreatic Diversion with Duodenal Switch (BPDS) versus Roux-en-Y Gastric Bypass (RYGB) has been attributed to the malabsorptive effects of BPDS. Increased weight loss after BPDS could also be underpinned by larger increases in energy expenditure. Hypothetically, the more radical reconfiguration of the small intestine in BPDS could result in an accentuated increase in meal associated thermogenesis (MAT). Female subjects (baseline mean age 40 years, mean BMI-55kg/m(2)) were assessed four years after randomization to BPDS (n = 6) or RYGB (n = 6). Energy expenditure (EE) and respiratory quotient (RQ) were measured by indirect calorimetry over 24 hours. A detailed protocol allowed for discrimination of basal metabolic rate (BMR), fasting EE and MAT as components of total energy expenditure (TEE) normalised for total and lean tissue by dual energy x-ray absorptiometry. Median weight loss at follow-up was 1.5-fold higher following BPDS relative to RYGB, resulting in respective median BMIs of 29.5 kg/m 2 (21.7 to 36.7) after BPDS and 37.8 kg/m(2) (34.1 to 45.7) after RYGB (p = 0.015). The BPDS group had a lower fat:lean ratio compared to the RYGB group (p = 0.009). Overall 24-hour TEE adjusted for total tissue was higher in the BPDS group, as were BMR, fasting EE and MAT (all p<0.05). Differences between RYGB and BPDS in BMR and TEE were nullified when normalised for lean mass. Postprandial RQ increased significantly but to a similar extent in both groups. Enhanced and prolonged MAT and lower fat:lean mass ratios after BPDS may explain relative increases in total energy expenditure as compared to RYGB.
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