R. Unger

Publications542
h-index120
Citations48,470
Highly Influential Citations1,113
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Lipotoxic heart disease in obese rats: implications for human obesity.
TLDR
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.
TLDR
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.
Lipotoxic diseases.
  • R. Unger
  • Biology, Medicine
    Annual review of medicine
  • 2002
TLDR
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
TLDR
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
TLDR
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
TLDR
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
TLDR
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.
TLDR
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.
TLDR
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*
TLDR
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.
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