Fructose induced lipogenesis: from sugar to fat to insulin resistance

  title={Fructose induced lipogenesis: from sugar to fat to insulin resistance},
  author={Varman T. Samuel},
  journal={Trends in Endocrinology \& Metabolism},
  • V. Samuel
  • Published 1 February 2011
  • Biology
  • Trends in Endocrinology & Metabolism

Fructose and hepatic insulin resistance

The current evidence shows that the fructose, but not glucose, component of dietary sugar drives metabolic complications and contradicts the notion that fructose is merely a source of palatable calories that leads to increased weight gain and insulin resistance.

Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease

The cellular mechanisms underlying hepatic fructose metabolism will likely reveal novel targets for the treatment of NAFLD, dyslipidemia, and hepatic insulin resistance, and fructose-containing sugars are a major source of excess calories, suggesting that a reduction of their intake has potential for the prevention ofNAFLD and other obesity-related diseases.

The role of the carbohydrate response element-binding protein in male fructose-fed rats.

It is suggested that targeting ChREBP may prevent fructose-induced hypertriglyceridemia but without the improvements in hepatic steatosis and hepatic insulin responsiveness.

The Role of Carbohydrate Response Element Binding Protein in Intestinal and Hepatic Fructose Metabolism

Understanding the mechanisms underlying intestinal and hepatic fructose metabolism is important for the treatment of metabolic syndrome and fructose malabsorption and restriction of excess fructose intake will be beneficial for preventing not only metabolic syndrome but also irritable bowl syndrome.

The Role of Dietary Sugars and De novo Lipogenesis in Non-Alcoholic Fatty Liver Disease

It is concluded that the use of hypercaloric, supra-physiological doses in intervention trials has been a major confounding factor and whether or not dietary sugars, including fructose, at typically consumed population levels, effect hepatic lipogenesis and NAFLD pathogenesis in humans independently of excess energy remains unresolved.

Fructose Metabolism and Relation to Atherosclerosis, Type 2 Diabetes, and Obesity

Current literature does not indicate that a normal consumption of fructose increases the risk of atherosclerosis, type 2 diabetes, or obesity more than consumption of other sugars, however, a high intake of fructose, particularly if combined with a high energy intake in the form of glucose/starch, may have negative health effects via DNL.

The role of fructose in metabolism and cancer

An overview of fructose metabolism and how it contrasts with that of glucose is presented and how excessive fructose consumption can affect de novo lipogenesis, insulin resistance, inflammation, and reactive oxygen species production.

Effects of chronic sugar consumption on lipid accumulation and autophagy in the skeletal muscle

The present results suggest that intramyocellular lipids and the pro-inflammatory signaling could contribute to the onset of insulin resistance and lead to the induction of autophagy, which could be an adaptive response to lipotoxicity.



Intermediary metabolism of fructose.

  • P. Mayes
  • Biology, Computer Science
    The American journal of clinical nutrition
  • 1993
Acute loading of the liver with fructose causes sequestration of inorganic phosphate in fructose-1-phosphate and diminished ATP synthesis, and the inhibition by ATP of the enzymes of adenine nucleotide degradation is removed and uric acid formation accelerates with consequent hyperuricemia.

Hepatic gene regulation by glucose and polyunsaturated fatty acids: a role for ChREBP.

A better understanding of the mechanisms by which glucose and fatty acids control hepatic gene expression may provide novel insight into the development of new therapeutic strategies for a better management of diseases involving blood glucose and/or disorders of lipid metabolism.

Inhibition of ADRP prevents diet-induced insulin resistance.

  • G. VarelaD. Antwi R. Ahima
  • Biology, Medicine
    American journal of physiology. Gastrointestinal and liver physiology
  • 2008
An important role for ADRP in the pathogenesis of diet-induced insulin resistance is demonstrated and insulin action in the liver was enhanced after ADRP ASO treatment, whereas muscle and adipose tissue were not affected.

Crucial role of a long-chain fatty acid elongase, Elovl6, in obesity-induced insulin resistance

Hepatic fatty acid composition is a new determinant for insulin sensitivity that acts independently of cellular energy balance and stress and could be a new therapeutic approach for ameliorating insulin resistance, diabetes and cardiovascular risks, even in the presence of a continuing state of obesity.

Mechanism of Hepatic Insulin Resistance in Non-alcoholic Fatty Liver Disease*

The hypothesis hepatic steatosis leads to hepatic insulin resistance by stimulating gluconeogenesis and activating PKC-ϵ and JNK1, which may interfere with tyrosine phosphorylation of IRS-1 and IRS-2 and impair the ability of insulin to activate glycogen synthase is supported.

Regulation of Hepatic Lipogenesis by the Transcription Factor XBP1

It is found that the transcription factor XBP1, a key regulator of the unfolded protein response, is required for the unrelated function of normal fatty acid synthesis in the liver.

Inhibition of protein kinase Cε prevents hepatic insulin resistance in nonalcoholic fatty liver disease

The hypothesis that PKCepsilon plays a critical role in mediating fat-induced hepatic insulin resistance and represents a novel therapeutic target for type 2 diabetes is supported.