Addendum to: Characterization of the resistance to the anorectic and endocrine effects of leptin in obesity-resistant rats fed a high-fat diet. Journal of Endocrinology 2004, 183 289-298

Tulipano, Giovanni; Vergoni, Anna Valeria; Soldi, D.; Ee, Müller

doi:10.1677/joe.1.05819e

Cited by 2 publications

(3 citation statements)

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“…Our results and those of others [21,31] demonstrate that at least 12 days or longer are required before the body weights of LFD and HFD mice and rats diverge. One possible explanation for the latency is that consumption of an HFD gradually induces changes in intestinal morphology and surface area, enterocyte function, and fatty acid transport such that the efficiency of nutrient absorption from the gut is increased [36,37].…”

Section: Discussionsupporting

confidence: 78%

“…Among these are the development of obesity with increased adiposity [4], and leptin and insulin resistance [1,21] characterized by reduced target cell sensitivity to leptin and insulin and increased circulating levels of the hormones. The increased body weights, adiposity and circulating hormones and glucose levels observed in the present study confirmed the expected phenotype of wild-type mice chronically consuming an HFD.…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that hyperleptinemia itself contributes to leptin resistance in animal models of obesity, possibly due to such events as ligand-induced down-regulation of the leptin receptor (ObR) [21][22][23][24] or to leptininduced generation of intracellular inhibitory signals [13]. One way to address the question of how circulating leptin and HFD interact over the long term in the development of obesity is to examine the effects of HFD in leptin-deficient mice with or without leptin replacement.…”

Section: Introductionmentioning

confidence: 99%

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High-fat diet-induced changes in body mass and hypothalamic gene expression in wild-type and leptin-deficient mice

Townsend

Lorenzi

Widmaier

2008

Endocr

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We tested whether diet-induced obesity results from increased energy consumption, is associated with changes in expression of genes involved in leptin signal transduction, and is altered by hyperleptinemia. C57BL/6 mice were fed a low-fat diet (LFD) or high-fat diet (HFD) for up to 15 weeks. HFD mice weighed significantly more than LFD controls by 3 weeks, despite consuming less energy. HFD mice had significantly greater leptin, insulin, and glucose levels than LFD mice, suggesting leptin and insulin resistance. Adiponectin levels declined with age but were unaffected by diet. HFD was associated with altered hypothalamic expression of genes whose products regulate the activity or nuclear translocation of STAT3, an important mediator of leptin actions. Expression of two isoforms of the leptin receptor decreased at 15 weeks in hypothalami of HFD mice in a tissue-specific manner. The type of fat (saturated versus unsaturated) did not influence weight gain on an HFD, but animals on LFD gained significantly more weight and adiposity if the dietary fat consisted mostly of saturated fats; this occurred despite no difference in energy consumption or absorption. Replacement of leptin to leptin-deficient ob/ob mice decreased hypothalamic leptin receptor expression and did not prevent HFD-induced weight gain. It is concluded that (1) increased energy consumption is not required for HFD-induced obesity in C57BL/6 mice, (2) HFD results in weight gain partly by modulating hypothalamic leptin-signaling pathways, (3) saturated fats induce weight gain even when total fat content of the diet is low, and (4) the effects of HFD are manifest in the presence or absence of circulating leptin.

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