Insulin-like growth factor I mediates high-fat diet-induced adipogenesis in Osborne-Mendel rats

Marques, Bianca; Hausman, Dorothy B.; Latimer, Amanda; Kras, Krystyna M.; Grossman, Barbara Mullen; Martin, Roy J.

doi:10.1152/ajpregu.2000.278.3.r654

Cited by 32 publications

(26 citation statements)

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“…ingly, neither IGF-I nor TNF-␣, previously shown to be upregulated in adipose tissue of high-fat-diet-fed rats (19,22), was among these. However, semiquantitative RT-PCR revealed a slight induction of these two factors after 1 wk of high-fat feeding.…”

Section: Resultsmentioning

confidence: 69%

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Gene expression profile of rat adipose tissue at the onset of high-fat-diet obesity

Pan

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

139

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Morbid obesity is the result of massive expansion of white adipose tissue (WAT) and requires recruitment of adipocyte precursor cells and their supporting infrastructure. To characterize the change in the expression profile of the preexisting WAT at the start of obesity, when adipocyte hypertrophy is present but hyperplasia is still minimal, we employed a cDNA subtraction screen for genes differentially expressed in epididymal fat pads harvested 1 wk after the start of a 60% fat diet. Ninety-six genes were upregulated by at least 50% above the WAT of control rats receiving a 4% fat diet. Of these genes, 30 had not previously been identified. Sixteen of the 96 genes, including leptin, adipocyte complement-related protein 30 kDa, and resistin, were predicted to encode a signal peptide. Ten of the 16 had been previously identified in other tissues and implicated in cell growth, proliferation, differentiation, cell cycle control, and angiogenesis. One was a novel gene. Twenty-nine novel fragments were identified. Thus, at the onset of high-fat-diet-induced obesity in rats, adipose tissue increases its expression of factors previously implicated in the expansion of nonadipocyte tissues and of several uncharacterized novel factors. The only one of these thus far characterized functionally was found to promote lipogenesis.

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Section: Resultsmentioning

confidence: 69%

“…Two adipocyte products previously implicated in preadipocyte maturation [IGF-I (19,16,24,28,32) and MCSF (17)] were not detected in our subtraction screen. IGF-I was increased 1.5-fold when semiquantified by RT-PCR, but MCSF could not be detected at this stage of the disorder.…”

Section: Discussionmentioning

confidence: 85%

Gene expression profile of rat adipose tissue at the onset of high-fat-diet obesity

Pan

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

139

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“…The transcription of IGF-1 in a tissue can reflect the level of IGF-1 protein synthesis 53 and, as in the case of interleukins, 54 IGF-1 has an autocrine-paracrine action. 55,56 IGF-1 57 In obese animals, this relationship may be sufficient to maintain low TG and glucose plasma concentrations without hyperinsulinism. On the contrary, IGF-1 and GLUT 4 gene expressions decreased in adult OF skeletal muscles and may confirm the lower insulin sensitivity of this tissue as compared to NF pigs.…”

Section: Discussionmentioning

confidence: 99%

Childhood obesity and insulin resistance in a Yucatan mini-piglet model: putative roles of IGF-1 and muscle PPARs in adipose tissue activity and development

et al. 2005

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OBJECTIVE:To explore metabolic and cellular modifications induced during childhood obesity, in a novel animal model of obese mini-piglets. DESIGN: A total of 10 four-month old Yucatan mini-pigs were followed from prepuberty to adulthood. Animals were divided into two groups. The first one had been overfed (OF) a western-type diet and the second one had been normally fed a control recommended human-type diet (NF). MEASUREMENTS: Plasma insulin-like growth factor 1 (IGF-1), insulin, leptin, nonesterified fatty acids, triglycerides (TGs) and glucose were determined at sexual maturity and at young adulthood. Quantitative gene expressions of peroxysome-proliferatoractivated receptors (PPARs), glucose transporter 4, insulin receptor, IGF-1, leptin and interleukin-6 (IL-6) in skeletal muscle, adipose tissue and liver were also measured at both stages. Adult insulin sensitivity was measured via euglycaemichyperinsulinaemic clamps. RESULTS: Increased body weight in adult OF pigs was associated with increased body size and low insulin sensitivity. Sexually mature OF pigs had higher IGF-1 plasma concentrations than their lean littermates (Po0.05). In the OF group, TGs and glucose were both decreased (Po0.05). Muscle PPARg and a in OF pubescent pigs as compared to NF pigs were 11 times higher and 20 times lower, respectively (Po0.01). CONCLUSION: Obesity and insulin resistance induced by overfeeding mini-pigs during development and puberty were not associated with the cluster of metabolic modifications frequently observed in their adult littermates. Increased IGF-1 concentrations and modifications of skeletal muscle PPAR (a and g) expressions may help the young obese pig to partially regulate its glycaemia and triglyceridaemia through an increase of fat mass, which maintains its high insulin sensitivity.

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“…An increase in fat cell size before the onset of adipocyte hyperplasia has been observed in diet-induced obese rats (47). Adipose tissue levels of TNF-␣ and IGF-I have been shown to be higher in both human and rodent obesity (45,87,105), but these paracrine factors have seemingly opposing effects on adipose tissue development. IGF-I induces both mitogenic and differentiation responses in preadipocyte cultures (178), whereas TNF-␣ inhibits the expression of adipogenic enzymes (184).…”

Section: E834mentioning

confidence: 99%

The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation

Frühbeck

Gómez-Ambrosi²,

Muruzábal

et al. 2001

American Journal of Physiology-Endocrinology and Metabolism

804

571

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The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation. Am J Physiol Endocrinol Metab 280: E827-E847, 2001.-The ability to ensure continous availability of energy despite highly variable supplies in the environment is a major determinant of the survival of all species. In higher organisms, including mammals, the capacity to efficiently store excess energy as triglycerides in adipocytes, from which stored energy could be rapidly released for use at other sites, was developed. To orchestrate the processes of energy storage and release, highly integrated systems operating on several physiological levels have evolved. The adipocyte is no longer considered a passive bystander, because fat cells actively secrete many members of the cytokine family, such as leptin, tumor necrosis factor-␣, and interleukin-6, among other cytokine signals, which influence peripheral fuel storage, mobilization, and combustion, as well as energy homeostasis. The existence of a network of adipose tissue signaling pathways, arranged in a hierarchical fashion, constitutes a metabolic repertoire that enables the organism to adapt to a wide range of different metabolic challenges, such as starvation, stress, infection, and short periods of gross energy excess. leptin; tumor necrosis factor-␣; interleukins; obesity; insulin resistance OVERVIEW Unraveling the diverse hormonal and neuroendocrine systems that regulate energy balance and body fat has been a long-standing challenge in biology, with obesity as an increasingly important public health focus (12). Adipose tissue is the body's largest energy reservoir. For example, an adult with 15 kg of body fat has Ͼ460 MJ (110,000 kcal) of lipid fuel stores, which could provide 8.37 MJ (2,000 kcal) daily for ϳ2 mo (75, 129). The primary role of adipocytes is to store triacylglycerol during periods of caloric excess and to mobilize this reserve when expenditure exceeds intake. Mature adipocytes are uniquely equipped to perform these functions. They possess the full complement of enzymes and regulatory proteins needed to carry out both lipolysis and de novo lipogenesis. In fat cells, the regulation of these processes is exquisitely responsive to hormones, cytokines, and other factors that are involved in energy metabolism (87). The ability to carry out these functions is acquired during embryonic development in preparation for the postnatal period, when an adipose energy reserve becomes necessary. Major expansion of the white adipocyte population is delayed until shortly after birth, although preadipocytes first appear late in embryonic life (22).The present review will focus on the evidence for the synthesis and secretion by white adipocytes of endocrine, paracrine, and autocrine signals implicated in energy balance regulation, with special reference to cytokines. The interactions between these adipose tissue-derived mediators and other neuroendocrine pathways will be examined. Furthermore, the metabolic alterations in adipose tissue signaling leading...

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Insulin-like growth factor I mediates high-fat diet-induced adipogenesis in Osborne-Mendel rats

Cited by 32 publications

References 26 publications

Gene expression profile of rat adipose tissue at the onset of high-fat-diet obesity

Gene expression profile of rat adipose tissue at the onset of high-fat-diet obesity

Childhood obesity and insulin resistance in a Yucatan mini-piglet model: putative roles of IGF-1 and muscle PPARs in adipose tissue activity and development

The adipocyte: a model for integration of endocrine and metabolic signaling in energy metabolism regulation

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