Document Type

Journal Article


Austin Publishing Group


School of Medical and Health Sciences




Edith Cowan University

McCusker Alzheimer’s Research Foundation

National Health and Medical Research Council


Martins, I. J. (2016). Appetite control with relevance to mitochondrial biogenesis and activation of post-prandial lipid metabolism in obesity linked diabetes. Annals of Obesity & Disorders, 1(3), 1-3.


In various communities in the developing and developed world the understanding of the ingestion of a healthy diet [1] and hepatic fat metabolism has become of critical importance to the treatment of obesity linked Type 2 diabetes that is now linked to various organ diseases [2]. In the developing world transition to healthy diets has become urgent to prevent insulin resistance [3,4] and the obesity pandemic [5-8]. The liver is the major organ for the metabolism of dietary fat and after consumption of a meal in healthy individuals the fat is rapidly metabolized by the liver. In obesity linked Type 2 diabetes the post-prandial metabolism of a fat meal by the liver is defective with fat transport to the adipocyte relevant to adipocyte and brain appetite centre dysfunction [9-11] (Figure 1). In obese and diabetic mice post-prandial lipid metabolism has been shown to be defective with defects in the appetite centre associated with hyperglycemia and hyperphagia. Activation of hepatic fat metabolism with restricted food intake in these rodent studies may be relevant to adipocyte lipid metabolism and adipocyte signals that relate to appetite control [12] are vital to the treatment of obesity linked diabetes [13].

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Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.