1.
The Role of Dietary Protein and Fat in Glycaemic Control in Type 1 Diabetes: Implications for Intensive Diabetes Management.
Paterson, M, Bell, KJ, O'Connell, SM, Smart, CE, Shafat, A, King, B
Current diabetes reports. 2015;(9):61
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Abstract
A primary focus of the management of type 1 diabetes has been on matching prandial insulin therapy with carbohydrate amount consumed. However, even with the introduction of more flexible intensive insulin regimes, people with type 1 diabetes still struggle to achieve optimal glycaemic control. More recently, dietary fat and protein have been recognised as having a significant impact on postprandial blood glucose levels. Fat and protein independently increase the postprandial glucose excursions and together their effect is additive. This article reviews how the fat and protein in a meal impact the postprandial glycaemic response and discusses practical approaches to managing this in clinical practice. These insights have significant implications for patient education, mealtime insulin dose calculations and dosing strategies.
2.
Alcohol-induced liver disease: when fat and oxidative stress meet.
Fernández-Checa, JC
Annals of hepatology. 2003;(2):69-75
Abstract
Reactive oxygen species (ROS) act as signaling intermediates regulating multiple cellular processes. The fate and disposal of the signaling species are determined by the actions of antioxidants, particularly glutathione (GSH). The mitochondrial pool of GSH (mGSH) arises from the transport of cytosol GSH by a specific mitochondrial carrier and is responsible for the maintenance of a healthy competent organelle. The depletion of mGSH upon impairment of the mitochondrial transport activity leaves mitochondria unprotected from damaging effects of ROS overgeneration within the mitochondrial electron transport chain. Tumor necrosis factor-alpha (TNF-alpha) has emerged as a key player in the progression of the alcohol-induced liver disease (ALD), and is known to target mitochondria. Key components of TNF signaling include sphingolipids, particularly ceramide generated from acidic sphingomyelinase activation serving as a source for gangliosides. In experimental models alcohol consumption enhances cholesterol levels and subsequent deposition into mitochondria resulting in selective decrease in the mGSH stores which is sufficient by itself to sensitize hepatocytes to TNF-alpha-mediated cell death. Thus, the combination of TNF-alpha overproduction, enhanced glycosphingolipid generation and selective mGSH depletion by alcohol intake cooperate making the liver sensitive to alcohol.