Metabolic programming of lipid profile and reproductive organs weight by leptin treatment on early life

Marques, Durval Santos; Gombar, Flavia Meireles; Alves-Pereira, Jorge Luiz; Sampaio, Francisco J.B.; Ramos, Cristiane da Fonte

doi:10.1590/s0102-86502010000100013

Cited by 4 publications

(4 citation statements)

References 14 publications

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“…Investigators using neonatal leptin treatment given to offspring of normally fed dams have shown increased adiposity and leptin and insulin resistance in offspring in later life [33–35]. The present result shows that the reverse can hold true.…”

Section: Discussionsupporting

confidence: 51%

The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

Beltrand

Sloboda

Connor

et al. 2012

Journal of Nutrition and Metabolism

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Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose, β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.

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Section: Discussionsupporting

confidence: 51%

The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

Beltrand

Sloboda

Connor

et al. 2012

Journal of Nutrition and Metabolism

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“…In fact, in certain rodent and human gliomas, the phosphoinositide-3-kinase (PI3K-Akt) pathway seems to activate ABCG2 transporters, whereas the loss of another signaling molecule phosphatase and tensin homologue deleted on chromosome 10 (PTEN) enhances ABCG2 expression [228,246]. In addition, specific pluripotent CSCs regulatory molecules, such as Thy-1, c-kit, Oct-4, and others maintains renewal and totipotency and are suspected to "cross-talk" with the transcriptional regulation of some MDR-ABC transporters such as ABCB1, ABCG2 and ABCC1 [246,247]. Further characterization of ABC transporters will clarify their role in the modulation of key regulatory pathways involved in stem cell biology.…”

Section: Abc Transporters In Cancer Stem Cellsmentioning

confidence: 99%

Revisiting the ABCs of Multidrug Resistance in Cancer Chemotherapy

Tiwari

Sodani²,

Dai³

et al. 2011

CPB

196

147

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The adenosine tri-phosphate binding cassette (ABC) transporters are one of the largest transmembrane gene families in humans. The ABC transporters are present in a number of tissues, providing protection against xenobiotics and certain endogenous molecules. Unfortunately, their presence produces suboptimal chemotherapeutic outcomes in cancer patient tumor cells. It is well established that they actively efflux antineoplastic agents from cancer cells, producing the multidrug resistance (MDR) phenotype. The inadequate response to chemotherapy and subsequent poor prognosis in cancer patients can be in part the result of the clinical overexpression of ABC transporters. In fact, one of the targeted approaches for overcoming MDR in cancer cells is that directed towards blocking or inhibiting ABC transporters. Indeed, for almost three decades, research has been conducted to overcome MDR through pharmacological inhibition of ABC transporters with limited clinical success. Therefore, contemporary strategies to identify or to synthesize selective "resensitizers" of ABC transporters with limited nonspecific toxicity have been undertaken. Innovative approaches en route to understanding specific biochemical role of ABC transporters in MDR and tumorigenesis will prove essential to direct our knowledge towards more effective targeted therapies. This review briefly discusses the current knowledge regarding the clinical involvement of ABC transporters in MDR to antineoplastic drugs and highlights approaches undertaken so far to overcome ABC transporter-mediated MDR in cancer.

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“…However, leptin concentrations in the milk progressively increased during lactation, suggesting that this change is related to differences in leptin production by epithelial cells in the mammary gland (50). In rats, the pup's immature stomach can absorb orally provided leptin (50), and early exposure to high leptin levels increases adult body weight (51). Leptin also seems to influence neuronal growth in the hypothalamus (52).…”

Section: Breast Milkmentioning

confidence: 99%

Perinatal Lack of Maternal IL-6 Promotes Increased Adiposity During Adulthood in Mice

Lager¹,

Asterholm²,

Schéle³

et al. 2011

Endocrinology

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The perinatal environment appears important in establishing metabolic phenotypes in adulthood. Mice deficient in IL-6 (IL-6(-/-)) tend to develop mature-onset obesity, but it is unknown whether perinatal exposure to IL-6 produced by the dam influences the metabolism of adult offspring. To address this issue, we monitored IL-6(-/-) offspring of IL-6(-/-) or IL-6(+/-) dams, as well as wild-type (WT) mice. At adult age, IL-6(-/-) mice weighed significantly more and had more body fat than WT mice, regardless of maternal genotype, and had lower insulin sensitivity. This phenotype was more pronounced in IL-6(-/-) offspring of IL-6(-/-) dams, because they gained weight significantly faster than IL-6(-/-) offspring of IL-6(+/-) dams and had more body fat and higher serum leptin levels at an earlier age. The leptin content was 2-fold higher in milk from IL-6(-/-) than WT dams. However, cross-fostering IL-6(-/-) mice with WT dams did not alter body weight, body composition, or adipocyte size at adult age compared with IL-6(-/-) mice fostered by IL-6(-/-) dams. Conversely, WT mice fostered by IL-6(-/-) dams weighed significantly more than those fostered by WT dams and had more body fat, larger adipocytes, and altered hypothalamic gene expression. We conclude that body fat of adult mice can be increased by perinatal exposure to factors affected by lack of maternal IL-6.

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Metabolic programming of lipid profile and reproductive organs weight by leptin treatment on early life

Cited by 4 publications

References 14 publications

The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

The Effect of Neonatal Leptin Antagonism in Male Rat Offspring Is Dependent upon the Interaction between Prior Maternal Nutritional Status and Post-Weaning Diet

Revisiting the ABCs of Multidrug Resistance in Cancer Chemotherapy

Perinatal Lack of Maternal IL-6 Promotes Increased Adiposity During Adulthood in Mice

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