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Lipotoxic heart disease in obese rats: implications for human obesity.
- Y. T. Zhou, P. Grayburn, R. Unger
- Medicine, BiologyProceedings of the National Academy of Sciences…
- 15 February 2000
Cardiac dysfunction in obesity is caused by lipoapoptosis and is prevented by reducing cardiac lipids and Troglitazone therapy lowered myocardial TG and ceramide and completely prevented DNA laddering and loss of cardiac function.
Glucagonocentric restructuring of diabetes: a pathophysiologic and therapeutic makeover.
It is concluded that glucose-responsive β cells normally regulate juxtaposed α cells and that without intraislet insulin, unregulated α cells hypersecrete glucagon, which directly causes the symptoms of diabetes, indicating that glucagon suppression or inactivation may provide therapeutic advantages over insulin monotherapy.
- R. Unger
- Biology, MedicineAnnual review of medicine
Evidence that leptin is a liporegulatory hormone that controls lipid homeostasis in nonadipose tissues during periods of overnutrition is reviewed and there is now substantial evidence that complications of human obesity may reflect lipotoxicity similar to that described in rodents.
Leptin therapy in insulin-deficient type I diabetes
- May-yun Wang, Lijun Chen, R. Unger
- Medicine, BiologyProceedings of the National Academy of Sciences
- 1 March 2010
It is shown that leptin therapy, like insulin, normalizes the levels of a wide array of hepatic intermediary metabolites in multiple chemical classes, including acylcarnitines, organic acids, amino acids, and acyl CoAs, and it lowers both lipogenic and cholesterologenic transcription factors and enzymes and reduces plasma and tissue lipids.
Making insulin-deficient type 1 diabetic rodents thrive without insulin
- Xinxin Yu, Byung-Hyun Park, May-yun Wang, Zhao V. Wang, R. Unger
- Biology, MedicineProceedings of the National Academy of Sciences
- 16 September 2008
It is suggested that leptin reverses the catabolic consequences of total lack of insulin, potentially by suppressing glucagon action on liver and enhancing the insulinomimetic actions of IGF-1 on skeletal muscle, and suggest strategies for making type 1 diabetes insulin-independent.
Lipotoxicity in the Pathogenesis of Obesity-Dependent NIDDM: Genetic and Clinical Implications
- R. Unger
- 1 August 1995
It is proposed that in uncomplicated obesity, increased lipid availability (FFA levels <1.5 mmol/1) induces both hyperinsulinemia and insulin resistance in parallel fashion, thereby maintaining normoglycemia.
Fatty acid-induced β cell apoptosis: A link between obesity and diabetes
In Zucker diabetic fatty (ZDF) rats, β cell apoptosis is induced by increased FFA via de novo ceramide formation and increased NO production, which is involved in FFA-induced apoptosis.
Lipotoxicity of beta-cells in obesity and in other causes of fatty acid spillover.
If leptin is deficient or if leptin receptors (Ob-R) are nonfunctional, this autoregulatory system does not operate, and triacylglycerol content rises in nonadipose tissues, providing a source of excess FAs that enter potentially toxic pathways of nonoxidative metabolism leading to apoptosis of certain tissues.
Fatty acid-induced beta cell apoptosis: a link between obesity and diabetes.
- M. Shimabukuro, Y. T. Zhou, M. Levi, R. Unger
- Biology, MedicineProceedings of the National Academy of Sciences…
In ZDF obesity, beta cell apoptosis is induced by increased FFA via de novo ceramide formation and increased NO production, which is involved in FFA-induced apoptosis.
Novel Form of Lipolysis Induced by Leptin*
In normal adipocytes leptin directly decreases FAS expression, increases PPARα and the enzymes of F FA oxidation, and stimulates a novel form of lipolysis in which glycerol is released without a proportional release of FFA.