“…Rat models previously exhibited reduced food intake as well as avoidance of high-fat diets [23]. In human, RYGB leads to a selective reduction of the reward value of fatty and sweet tastes [24]. Previous studies showed postoperatively enhanced post-prandial satiation, which was associated with enhanced release of satiety gut hormones such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine (PYY) [25].…”
It appears reasonable that multidisciplinary treatment including surgical alternatives should be concerned for all morbidly obese patients, considering high rate of failure of conservative medical therapy in this setting.
“…Rat models previously exhibited reduced food intake as well as avoidance of high-fat diets [23]. In human, RYGB leads to a selective reduction of the reward value of fatty and sweet tastes [24]. Previous studies showed postoperatively enhanced post-prandial satiation, which was associated with enhanced release of satiety gut hormones such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine (PYY) [25].…”
It appears reasonable that multidisciplinary treatment including surgical alternatives should be concerned for all morbidly obese patients, considering high rate of failure of conservative medical therapy in this setting.
“…Miras et al [36] retrospectively analysed data from a consecutive series of 84 patients with T2DM that had underwent bariatric surgery over a 12-18-month period. A cohort of 32 patients had albuminuria at baseline, and a mean 3.5-fold decrease in post-operative ACR was recorded at follow-up resulting in all 32 patients reverting to normoalbuminuria.…”
Progressive renal impairment (diabetic kidney disease (DKD)) occurs in upwards of 40 % of patients with obesity and type 2 diabetes mellitus (T2DM) and is a cause of significant morbidity and mortality. Means of attenuating the progression of DKD focus on amelioration of risk factors. Visceral obesity is implicated as a causative agent in impaired metabolic and cardiovascular control in T2DM, and various approaches primarily targeting weight have been examined for their impact on markers of renal injury and dysfunction in DKD. The current report summarises the evidence base for the impact of surgical, lifestyle and pharmacological approaches to weight loss on renal end points in DKD. The potential for a threshold of weight loss more readily achievable by surgical intervention to be a prerequisite for renal improvement is highlighted. Comparing efficacious non-surgical weight loss strategies with surgical strategies in appropriately powered and controlled prospective studies is a priority for the field.
“…Diabetic kidney disease is a result of microvascular damage to the renal glomeruli and appears for most parts to be progressive. After bariatric surgery, an improvement in kidney damage can be demonstrated with improved microalbuminuria [Miras et al 2012a] and albuminuria [Iaconelli et al 2011]. Halting the process of endorgan damage is vital in treating diabetes.…”
Section: Changes In Inflammation and Changes In Endorgan Damagementioning
Abstract:The obesity epidemic contributes to approximately 44% of the world's type 2 diabetes burden. Bariatric surgery is an effective treatment for type 2 diabetes mellitus in patients with morbid obesity as it improves glycaemia, blood pressure, lipids and inflammation. This review describes the evidence supporting the addition of bariatric surgery to the treatment algorithms used by diabetologists. We emphasize the need to view bariatric surgery as an adjuvant therapy which should not be used instead of but rather together with best medical therapy.
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