Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance. Focus on "Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding," by Shapiro et al.

@article{Vasselli2008FructoseinducedLR,
  title={Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance. Focus on "Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding," by Shapiro et al.},
  author={Joseph R. Vasselli},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2008},
  volume={295 5},
  pages={
          R1365-9
        }
}
  • J. Vasselli
  • Published 1 November 2008
  • Medicine
  • American journal of physiology. Regulatory, integrative and comparative physiology
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References

SHOWING 1-10 OF 80 REFERENCES

Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding.

TLDR
The data indicate that chronic fructose consumption induces leptin resistance prior to body weight, adiposity, serum leptin, insulin, or glucose increases, and this fructose-induced leptin resistance accelerates high-fat induced obesity.

Role of fat amount and type in ameliorating diet‐induced obesity: insights at the level of hypothalamic arcuate nucleus leptin receptor, neuropeptide Y and pro‐opiomelanocortin mRNA expression

TLDR
Examination of the effects of dietary fat amount and types on fat storage and hypothalamic gene expression in the mouse model of chronic diet‐induced obesity found it to be a major regulator of body adiposity.

Leptin resistance and the response to positive energy balance

Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism.

  • P. Havel
  • Medicine, Biology
    Nutrition reviews
  • 2005
TLDR
This review examines the available data on the effects of dietary fructose on energy homeostasis and lipid/carbohydrate metabolism and suggests an endocrine mechanism by which it induces a positive energy balance.

Leptin levels reflect body lipid content in mice: Evidence for diet-induced resistance to leptin action

TLDR
It is found that high-fat diet evokes a sustained increase in circulating leptin in both normal and transgenic mice, with leptin levels accurately reflecting the amount of body lipid across a broad range of body fat.

The role of leptin in human physiology.

In humans, the relative long-term constancy of body weight, the difficulty of successfully sustaining intentional weight loss, and the metabolic and behavioral alterations that accompany weight cha...

Overfeeding rapidly induces leptin and insulin resistance.

TLDR
A paradoxical and rapid collapse of the leptin system in response to nutrient excess is demonstrated and this partial failure is tightly coupled with the onset of insulin resistance.

Elevated leptin: consequence or cause of obesity?

  • P. ScarpaceYi Zhang
  • Biology, Medicine
    Frontiers in bioscience : a journal and virtual library
  • 2007
TLDR
An important role for elevated leptin is suggested in the development of leptin resistance and obesity, especially in today's society with an overabundance of readily available high caloric food.

Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus.

TLDR
It is concluded that HL feeding induces a local proinflammatory status in the hypothalamus, which results in impaired anorexigenic insulin signaling, which leads to a reduced caloric intake and weight loss.

Leptin receptor, NPY, POMC mRNA expression in the diet-induced obese mouse brain

...