Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

Férézou-Viala, Jacqueline; Roy, Anne-France; Sérougne, Colette; Gripois, D.; Parquet, Michel; Bailleux, Virginie; Gertler, Arieh; Delplanque, Bernadette; Djiane, Jean; Riottot, Michel; Taouis, Mohammed

doi:10.1152/ajpregu.00117.2007

Cited by 167 publications

(165 citation statements)

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“…After delivery, HF dams lost relatively more weight than did C dams, mainly during the second half of the lactation Adaptation to lactation in a model of obesity O Zagoory-Sharon et al period, and then the body weight became identical in the two groups at the end of the weaning period'. 53 Overall, these patterns of weight differences are very similar to those described in the current study, in which OLETF rats were much heavier than LETO controls as NP and on Lac1, although this difference dramatically decreased on Lac15 and 22 (Table 1). This similarity suggests that the pattern of OLETF adaptation to lactation may reflect their general hyperphagia-obesity phenotype, rather than, or possibly, in addition to, its specific CCK-1 mutant status.…”

Section: Discussionsupporting

confidence: 86%

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

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Objective: To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage. Design: Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning. Measurements: We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined. Results: Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters. Conclusions: Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.

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Section: Discussionsupporting

confidence: 86%

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

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“…Some studies in rodents have assessed influences of maternal high-energy diets using only a short time window, generally less than 14 days prior to mating or only during gestation and/or lactation, and have generally failed to achieve obesity in the dam [16,19,20,[24][25][26]. A few, using a prolonged feeding period to induce obesity [17,27,28], have generally switched from a high-energy diet to a control diet postdelivery [28], potentially inducing changes of the milk composition [29]. Since lactation may be a critical period for neonates in the programming of obesity, these protocols may affect the offspring phenotype [30].…”

Section: Discussionmentioning

confidence: 99%

“…Studies from our laboratories and others have shown that a maternal diet rich in animal fat during gestation and lactation leads to the development of an offspring phenotype with characteristics of the metabolic syndrome even when offspring are reared on a normal diet [16][17][18][19][20]. However, these dietary manipulations were made only during the short period of gestation and lactation and rodents fed a diet rich in fat alone are generally resistant to the development of obesity [16].…”

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confidence: 99%

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

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Aims/hypothesis Accumulating evidence suggests that maternal obesity may increase the risk of metabolic disease in the offspring. We investigated the effects of established maternal diet-induced obesity on male and female offspring appetite, glucose homeostasis and body composition in rats. Methods Female Wistar rats were fed either a standard chow (3% fat, 7% sugar [wt/wt]) or a palatable obesogenic diet (11% fat, 43% sugar [wt/wt]) for 8 weeks before mating and throughout pregnancy and lactation. Male and female offspring of control and obese dams were weaned on to standard chow and assessed until 12 months of age. Results At mating, obese dams were heavier than control with associated hyperglycaemia and hyperinsulinaemia. Male and female offspring of obese dams were hyperphagic (p<0.0001) and heavier than control (p<0.0001) until 12 months of age. NEFA were raised at 2 months but not at 12 months. At 3 months, OGTT showed more pronounced alteration of glucose homeostasis in male than in female offspring of obese animals. Euglycaemic-hyperinsulinaemic clamps performed at 8 to 9 months in female and 10 to 11 months in male offspring revealed insulin resistance in male offspring of obese dams (p<0.05 compared with control). Body compositional analysis at 12 months also showed increased fat pad weights in male and female offspring of obese animals. Conclusions/interpretation Diet-induced obesity in female rats leads to a state of insulin resistance in male offspring, associated with development of obesity and increased adiposity. An increase in food intake may play a role.

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“…The proximal occlusion cuff (O-cuff) constricts the tail artery while the distal VPR cuff measures the change in tail artery volume when blood flow resumes as the O-cuff deflates. This system has been validated in a number of studies [14,15,17] . These measurements were performed in a room maintained at 31 °C so as to ensure adequate blood flow through the tail to improve the signal at the VPR transducer.…”

Section: Experimental Designmentioning

confidence: 99%

“…In recent years, a new technique for measuring blood pressure in conscious rats using a volume pressure recording system has been validated in a number of studies [14,15] . Longterm oral administration of (±)doxazosin (8 mg/kg for 12 weeks) in the rat was also reported in a study by Yono et al [16] .…”

Section: Introductionmentioning

confidence: 99%

(−)Doxazosin is a necessary component for the hypotensive effect of (±)doxazosin during long-term administration in conscious rats

Zhao

Kong

et al. 2013

Acta Pharmacol Sin

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Aim: Doxazosin is a racemic mixture of (-)doxazosin and (+)doxazosin that is currently used as an add-on therapy for hypertension. In this study we investigated the contribution of each enantiomer to the hypotensive action of long-term administration of (±)doxazosin in conscious rats. Methods: Blood pressure of conscious SD rats was measured using a volume pressure recording system. The rats were orally administered (-)doxazosin, (+)doxazosin, or (±)doxazosin (8 mg·kg -1 ·d -1 ) for 12 weeks. Plasma concentrations of the agents were analyzed with HPLC. The effect of the agents on α 1 -adrenoceptor was examined in isolated rat caudal artery preparations. Results: Treatment of conscious rats with a single dose of (±)doxazosin (8 mg/kg) did not affected DBP and MBP, but significantly decreased SBP by 11.9% 4 h after the administration. Long-term treatment of conscious rats with (±)doxazosin significantly decreased SBP, DBP and MBP with a maximal decrease of SBP by 29.3% 8 h after the last administration. The rank order of the hypotensive actions caused by long-term treatment in conscious rats was (±)doxazosin>(+)doxazosin>>(-)doxazosin. However, the pK B values for inhibiting NA-induced contraction of isolated rat caudal artery were (+)doxazosin (8.995)>(±)doxazosin (8.694)>(-)doxazosin (8.032). The plasma concentrations of (-)doxazosin, (+)doxazosin, and (±)doxazosin were 18.26±3.55, 177.11±20.66, and 113.18±13.21 ng/mL, respectively, 8 h after the last administration of these agents. Conclusion: Long-term treatment with (±)doxazosin produces potent hypotensive action in conscious rats that seems to result from synergic interaction of the two enantiomers.

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Long-term consequences of maternal high-fat feeding on hypothalamic leptin sensitivity and diet-induced obesity in the offspring

Cited by 167 publications

References 50 publications

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

(−)Doxazosin is a necessary component for the hypotensive effect of (±)doxazosin during long-term administration in conscious rats

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