Nutrient regulation of pancreatic β-cell function in diabetes: problems and potential solutions

Flatt, Peter R.; Green, Brian

doi:10.1042/bst0340774

Cited by 13 publications

(7 citation statements)

References 55 publications

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“…It has been demonstrated that GLP-1 concentration in serum is increased in normal weight people after a meal, but not in morbidly obese patients [79]. Furthermore, GLP-1 has been also shown to promote satiety and decrease energy intake through its interaction with its receptors in the brain [80,81]. In a study by Pereferrer et al, baseline GLP-1 levels in non-obese rats were lower than those of obese animals, while its levels post-sleeve gastrectomy in obese rats have been shown to be lower than pre-interventional levels [82].…”

Section: Gastric Emptyingmentioning

confidence: 97%

Morbid Obesity and Sleeve Gastrectomy: How Does It Work?

et al. 2010

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Laparoscopic sleeve gastrectomy is known to be a safe and effective procedure for treating morbid obesity and is performed with increasing frequency both in Europe and the USA. Despite its broad use, many questions about the remaining gastric tube diameter, its long-term efficacy, its effects on gastric emptying, and the hormones involved still remain to be answered. In order to use such a relatively new surgical procedure wisely, it is essential for every surgeon and physician to understand how sleeve gastrectomy acts in obesity and what its potential benefits on the patients' metabolism are. This review focuses on the most important pathophysiologic questions referred to sleeve gastrectomy on the literature so far, in an attempt to evaluate the different issues still pending on the subject.

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Section: Gastric Emptyingmentioning

confidence: 97%

Morbid Obesity and Sleeve Gastrectomy: How Does It Work?

et al. 2010

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“…No single lesion can account for MS or its associated diseases [St. Pierre et al, 2005;Flatt and Green, 2006]. However, gene expression studies have shown that there is a coordinate reduction in oxidative gene activities along with increased expression of several other genes in type 2 diabetes [Vechoor et al, 2002].…”

Section: Oxidative Stress Mitochondrial Damage and Type 2 Diabetesmentioning

confidence: 99%

Metabolic syndrome and mitochondrial function: Molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function

Nicolson

2007

J of Cellular Biochemistry

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Metabolic syndrome consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart disease. One of the defects in metabolic syndrome and its associated diseases is excess cellular oxidative stress (mediated by reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to mitochondrial components, resulting in reduced efficiency of the electron transport chain. Recent evidence indicates that reduced mitochondrial function caused by ROS/RNS membrane oxidation is related to fatigue, a common complaint of MS patients. Lipid replacement therapy (LRT) administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial and other cellular membrane functions and reduce fatigue. Recent clinical trials have shown the benefit of LRT plus antioxidants in restoring mitochondrial electron transport function and reducing moderate to severe chronic fatigue. Thus LRT plus antioxidant supplements should be considered for metabolic syndrome patients who suffer to various degrees from fatigue.

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“…In contrast, the mutant enzyme was significantly less stable compared with wild-type CEL. A (35,36). Furthermore, it was shown to stimulate ␤-cell neogenesis, growth, and differentiation in rodents and tissue culture and to inhibit ␤-cell apoptosis in vitro.…”

Section: Diabetes and Pancreatic Exocrine Dysfunction Due To Mutationmentioning

confidence: 99%

Is Pancreatic Diabetes (Type 3c Diabetes) Underdiagnosed and Misdiagnosed?

et al. 2008

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Exocrine pancreatic insufficiency is frequently associated with diabetes, with high prevalence in both insulin-dependent or insulin-independent patients. Exocrine pancreatic failure has often been perceived as a complication of diabetes. In contrast, recent clinical observations lead to the notion that nonendocrine pancreatic disease is a critical factor for development rather than a sequel to diabetes. The incidence of diabetes caused by exocrine pancreatic disease appears to be underestimated and may comprise 8% or more of the general diabetic patient population. Nonendocrine pancreas disease can cause diabetes by multiple mechanisms. Genetic defects have been characterized, resulting in a syndrome of both exocrine and endocrine failure. Regulation of β-cell mass and physiological incretin secretion are directly dependent on normal exocrine function. Algorithms for diagnosis and therapy of diabetes should therefore address both endocrine and exocrine pancreatic function.

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Nutrient regulation of pancreatic β-cell function in diabetes: problems and potential solutions

Cited by 13 publications

References 55 publications

Morbid Obesity and Sleeve Gastrectomy: How Does It Work?

Morbid Obesity and Sleeve Gastrectomy: How Does It Work?

Metabolic syndrome and mitochondrial function: Molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function

Is Pancreatic Diabetes (Type 3c Diabetes) Underdiagnosed and Misdiagnosed?

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