Relationships among maternal backfat depth, plasma adipokines and the birthweight of piglets (original) (raw)
The Journal of physiology, 2004
Low birth weight is associated with altered adipose tissue deposition and regulation of leptin production. This study determined the effects of naturally occurring variations in birth weight in pigs on postnatal growth patterns, body fat depth and plasma leptin and other hormone concentrations. Low (< 1.47 kg) and high (> 1.53 kg) birth weight piglets were studied at 3 months (juvenile; n= 47) and 12 months of age (young adult; n= 17). At each age, arterial and venous catheters were inserted under general anaesthesia. Plasma leptin, cortisol, glucose, insulin and catecholamine concentrations were determined in basal blood samples. Body fat depth was measured by ultrasound at 12 months of age. Overall, adult fat depth was greater in low compared to high birth weight pigs and increased fat depth was associated with thinness at birth and poor early growth rates. These effects were strongest in females. Fat depth was related to current weight only in males. Compared to high birth ...
animal, 2008
With genetic selection, the increase in litter size has led to higher variation in within-litter birth weights in pigs. This has been associated with a reduction in mean birth weights and a rise in the proportion of piglets weighing less than 1 kg at birth. Low birth weight pigs exhibit lower postnatal growth rates and feed efficiency, which may be explained by an inadequate digestion and/or nutrient use as a consequence of prenatal undernutrition. It is now documented that there is a relationship between birth weight and subsequent pattern of growth and development of tissues and organs. During the neonatal period, the rapid somatic growth is accompanied by tremendous anatomical, physiological and chemical composition changes. The present review focuses primarily on the influence of low birth weight on adipose tissue and the gastrointestinal tract growth and development during the suckling period. The importance of the somatotropic axis, insulin, thyroid hormones, glucocorticoids, epidermal growth factor and leptin in the regulation of these developmental processes is also considered.
Differentiation, 2011
Intra-uterine growth retardation in piglets is associated to neonatal losses and a greater susceptibility to fat deposition in the long term. Dietary l-arginine supplementation to gilts during early gestation has been proposed as a way to enhance fetal survival. This study aims to investigate the effects of variation in fetal growth within litters and dietary l-arginine treatment during early gestation in pregnant sows on expression levels of several genes involved in early adipose tissue development and lipid deposition in the fetuses. At day 75 of pregnancy, sows fed a standard gestation diet throughout pregnancy and sows fed 26g L-arginine daily from days 14 to 28 of gestation in supplement to the standard diet were sacrificed. Six pairs of littermates in each dietary group with the smallest or the heaviest fetal weights within each litter were collected (total: 24 fetuses). Expression levels of DLK1/PREF1 and FZD7 were significantly greater in subcutaneous backfat of the smallest fetuses. Conversely, transcriptional adipogenic regulators PPARG, SREBP1, and CEBPA, and genes involved in terminal adipocytic differentiation LPL, ME1, and FABP4 were less expressed in those piglets. Fetal weight has no effect on expression levels of genes involved in cell cycle progression and DNA content in subcutaneous adipose tissue. Maternal dietary L-arginine treatment did not affect subcutaneous adipose tissue features in 75-day old fetuses. The gene expression changes observed in the smallest fetuses are likely associated to a lower body fat content at birth, and could predispose to catch-up fat growth during the postnatal period.
Endocrinology, 2003
We have investigated the factors regulating leptin synthesis, fat deposition, and circulating leptin concentrations in fetuses of well nourished ewes in late pregnancy. Vascular catheters were surgically inserted in 17 pregnant ewes and their fetuses at 103-120 d gestation (term ؍ 147 ؎ 3 d). Ewes were fed a diet providing either 100% (control; n ؍ 9) or approximately 155% (well fed; n ؍ 8) of the maintenance energy requirements and fetal perirenal and interscapular fat depots were collected at 139 -141 d gestation. There was a significant relationship between the relative mass of fetal unilocular fat and fetal glucose (relative mass of unilocular fat, 1.14; fetal glucose, ؉0.16; r ؍ 0.50; P < 0.04; n ؍ 17), but not insulin, concentrations in the control and well-fed groups. In contrast to the controls, there was a positive relationship between the relative abundance of leptin mRNA and fetal insulin, but not glucose, concentrations in fetal perirenal adipose tissue in the well-fed group. A moderate increase in maternal nutrition also resulted in a strong reciprocal relationship between uncoupling protein 1 and leptin expression in fetal perirenal adipose tissue in late gestation (well-fed group: uncoupling protein 1 mRNA:18S rRNA, ؊0.51; leptin mRNA:-actin mRNA, ؉1.53; r ؍ 0.80; P < 0.02; n ؍ 8). These studies provide evidence that fetal glucose and insulin differentially regulate fetal fat deposition and leptin mRNA expression within the fetal perirenal fat depot in the well nourished animal during late gestation. Abbreviations: GLUT, Glucose transporter; ME, metabolizable energy; PAT, perirenal adipose tissue; SSC, saline sodium citrate; UCP1, uncoupling protein 1.
Abundance of leptin mRNA in fetal adipose tissue is related to fetal body weight
Journal of Endocrinology, 1999
Leptin mRNA was measured in adipose tissue of fetal sheep by reverse transcription polymerase chain reaction (RTPCR). Abundance of leptin mRNA relative to β-actin mRNA in fetal perirenal adipose tissue increased (P<0.02) with gestation, being higher at 144 d (0.73 ± 0.10, n=5) than at 90-91 d (0.40 ± 0.08, n=6) or 125 d (0.40 ± 0.04, n=5) gestation (term ~147-150 d). There was a positive relationship between relative abundance of leptin mRNA (y) and fetal body weight (x) between 90 and 144 d gestation (r 2 =0.27, P<0.01). The slope of the linear dependence of leptin mRNA on fetal weight was 15-fold greater (P<0.001) at 90-91d (y = 2.81x -1.1, n=6, r 2 =0.71, P<0.025) than between 125-144 d gestation (y = 0.195x -0.15, n=16, r 2 =0.39, P<0.01). Thus the leptin synthetic capacity of fetal adipose tissue appears to increase in late gestation but this is accompanied by constraint of its sensitivity to fetal body weight. We hypothesise that leptin synthesis in fetal adipose tissue is related to fetal nutrient supply and growth rate.
Placenta, 2010
This study investigated the development of adipose tissue in the guinea pig and the impact of maternal undernutrition on the structural and functional characteristics of perirenal adipose tissue in the dam and fetus. Date-mated guinea pigs were provided with either ad libitum feed (Control, C) or 85% of food intake per body weight of the Controls (Undernutrition, UN). Maternal (C, n ¼ 6; UN, n ¼ 7) perirenal adipose tissue (PAT) was collected at 60 d gestation and fetal PAT was collected at 50 d (C, n ¼ 4) and 60 d (C, n ¼ 8 and UN, n ¼ 7) gestation (term, 69 d). The expression of stearoyl-CoA desaturase (SCD-1), fatty acid synthase (FAS), lipoprotein lipase (LPL), leptin and glycerol 3 phosphate dehydrogenase (G3PDH) mRNA and glucose transporters 1 and 4 (GLUT1 and GLUT4) was determined by Real Time PCR. There was no effect of maternal UN on total or relative PAT mass in the pregnant dam. There was an increase in G3PDH, but not LPL, leptin, FAS or GLUT4 mRNA expression, in UN dams compared to Controls (P < 0.05). In the fetal guinea pig there was no effect of maternal UN on total or relative PAT mass, however, the UN fetuses had a higher percentage of larger lipid locules in their PAT compared to Controls (P < 0.05). The expression of FAS, LPL, SCD-1, leptin, G3PDH and GLUT4 mRNA in PAT was not different between the Control and UN fetuses. These results support previous studies which have demonstrated that maternal undernutrition is associated with an increased accumulation of visceral adipose tissue in utero, and extend them by showing that maternal undernutrition results in early changes in the size distribution of lipid locules in visceral fat depots that precede changes in lipogenic gene expression.
Biology
Intrauterine growth restriction (IUGR) and later obesity and metabolic disorders have classically been associated with maternal malnutrition, but most cases of IUGR are related to placental insufficiency. The current study, using a swine model for IUGR and obesity, aimed to determine the interaction of birth weight (categorized as low birth weight [LBW] or normal birth-weight [NBW]) and postnatal diet (categorized as maintenance diet [MD] or fattening diet [FD]) on body weight, adiposity and metabolic traits. FD induced higher body weight and adiposity (both p < 0.0001), with higher fructosamine levels (p < 0.005) and a trend toward higher HOMA-β index (p = 0.05). NBW pigs remained heavier than LBW pigs during the early juvenile period (p < 0.005), but there were no differences at later stages. There were no differences in metabolic traits during juvenile development, but there were differences in adulthood, when LBW pigs showed higher glucose and lower insulin levels than ...
European Journal of Nutrition, 2012
Aim This study investigated whether dietary protein intake less (50%) or greater (250%) than requirements throughout gestation differently affects offspring body composition and cellular properties of skeletal muscle and subcutaneous adipose tissue (SCAT). Methods Primiparous gilts were fed iso-energetic diets containing adequate (22 AP), high (21 HP), or low (19 LP) protein contents. Newborn (n = 166) and weanling piglets cross-fostered to sows fed a standard diet (day 28; n = 83) were examined by morphological, biochemical, histological, and molecular analyses of the body, SCAT, and semitendinosus, longissimus, biceps femoris muscles. Results Lowered birth weight (BW) in response to the HP and LP diets (p \ 0.01) resulted from decreases in all body constituents in LP, and mainly from reduced body fat in HP piglets (p \ 0.05). In the light BW class within litters, HP piglets exhibited a greater percentage of muscle tissue (p \ 0.05) than LP piglets. Less SCAT mass in HP and LP piglets resulted from reduced (p \ 0.05) number, but not the size of adipocytes. The LP diet adversely affected myogenesis and muscular differentiation derived from less (p \ 0.01) primary and secondary myofibers, lower creatine kinase activity (p \ 0.05), less IGF2 mRNA (p \ 0.10), and greater expression of the embryonic myosin heavy chain isoform (p \ 0.01). Catch-up growth of LP but not HP pigs until day 28 increased body fat (p = 0.01). Despite compensated muscle growth in LP piglets, the deficit in myofiber number remained. Conclusion Poor intrauterine environment by limited and excess protein supply retards fetal growth, but only limited protein supply impairs myogenesis, persistently restricts muscle growth potential, and favors obesity at infancy.
Expression in the Perirenal Adipose Tissue of Late Gestation Fetal Sheep
Placental restriction (PR) of fetal growth results in a low birth weight and an increased visceral fat mass in postnatal life. We have investigated whether PR alters expression of genes which regulate adipogenesis (IGF1, IGF1R, IGF2, IGF2R, PPAR , RXR ), adipocyte metabolism (LPL, G3PDH, GAPDH) and adipokine signalling (leptin, adiponectin) in visceral adipose tissue before birth. PR was induced by removal of the majority of endometrial caruncles in non pregnant ewes prior to mating. Fetal blood samples were collected from 116d gestation and perirenal visceral adipose tissue (PAT) collected from PR and control fetuses at 145d. PAT gene expression was measured by qRT-PCR. PR fetuses had a lower weight (PR 2.90 ± 0.32 kg; Control, 5.12 ± 0.24 kg; P<0.0001), mean gestational arterial PO 2 (P<0.0001), plasma glucose (P<0.01) and insulin concentrations (P<0.02), than Controls. The expression of IGF1 mRNA in PAT was lower in the PR fetuses (PR 0.332 ± 0.063; Control 0.741 ± 0.083; P<0.01). Leptin mRNA expression in PAT was also lower in PR fetuses (PR 0.077 ± 0.009; Control, 0.115 ± 0.013; P<0.05), although there was no difference in the expression of other adipokine or adipogenic genes in PAT between PR and control fetuses. Thus restriction of placental and hence fetal substrate supply results in decreased IGF1 and leptin expression in fetal visceral adipose tissue which may alter the functional development of the perirenal fat depot and contribute to altered leptin signalling in the growth restricted new born and the subsequent emergence of an increased visceral adiposity. Rosberg S. Longitudinal follow-up of growth in children born small for gestational age. Acta Paediatr 82: 438-443, 1993. 3. Alkalay AL GJ, Pomerance JJ. Evaluation of neonates born with intrauterine growth retardation: review and practice guidelines. J Perinatol 18: 142-151, 1998. 4. Ambrosini G, Nath AK, Sierra-Honigmann MR, and Flores-Riveros J. Transcriptional activation of the human leptin gene in response to hypoxia. Involvement of hypoxia-inducible factor 1. Inhibition of p38MAPK Increases Adipogenesis From Embryonic to Adult Stages. Diabetes 55: 281-289, 2006. 6. Barker DJ, Hales CN, Fall CH, Osmond C, Phipps K, and Clark PM. Type 2 (noninsulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia 36: 62-67, 1993. 7. Bavdekar A, Yajnik CS, Fall CH, Bapat S, Pandit AN, Deshpande V, Bhave S, Kellingray SD, and Joglekar C. Insulin resistance syndrome in 8-year-old Indian children: small at birth, big at 8 years, or both? Diabetes 48: 2422-2429, 1999. 8. Circulating insulin-like growth factors (IGFs), IGF-binding proteins (IGFBPs) and tissue mRNA levels of IGFBP-2 and IGFBP-4 in the ovine fetus. J Endocrinol 145: 545-557, 1995. 11. Considine RV, Nyce MR, Morales LM, Magosin SA, Sinha MK, Bauer TL, Rosato EL, Colberg J, and Caro JF. Paracrine stimulation of preadipocyte-enriched cell cultures by mature adipocytes. Am J Physiol Endocrinol Metab 270: E895-899, 1996. 12. Curhan GC, Willett WC, Rimm EB, Spiegelman D, Ascherio AL, and Stampfer MJ. Birth weight and adult hypertension, diabetes mellitus, and obesity in US men. Circulation 94: 3246-3250, 1996. 13. Lamb. Endocrinology 148: 1350-1358, 2007. 14. De Blasio MJ, Gatford KL, Robinson JS, and Owens JA. Placental restriction of fetal growth reduces size at birth and alters postnatal growth, feeding activity, and adiposity in the young lamb. Am J Physiol Regul Integr Comp Physiol 292: R875-886, 2007. 15. Economides D, Nicolaides K, and Campbell S. Metabolic and endocrine findings in appropriate and small for gestational age fetuses. J Perinat Med 19: 97-105, 1991. 16. Edwards LJ, Symonds ME, Warnes KE, Owens JA, Butler TG, Jurisevic A, and McMillen IC. Responses of the fetal pituitary-adrenal axis to acute and chronic hypoglycemia during late gestation in the sheep. Endocrinology 142: 1778-1785, 2001. 17. Ehrhardt RA, Bell AW, and Boisclair YR. Spatial and developmental regulation of leptin in fetal sheep. DJ. Size at birth, childhood growth and obesity in adult life. Int J Obes Relat Metab Disord 25: 735-740, 2001. 20. Faust IM, Johnson PR, Stern JS, and Hirsch J. Diet-induced adipocyte number increase in adult rats: a new model of obesity. Am J Physiol Endocrinol Metab 235: E279-286, 1978. 21. Fitzhardinge PM and Steven EM. The small-for-date infant. I. Later growth patterns. Pediatrics 49: 671-681, 1972. 22. Gong DW, Bi S, Pratley RE, and Weintraub BD. Genomic structure and promoter analysis of the human obese gene. J Biol Chem 271: 3971-3974, 1996. 23. Greenwood PL, Hunt AS, Hermanson JW, and Bell AW. Effects of birth weight and postnatal nutrition on neonatal sheep: I. Body growth and composition, and some aspects of energetic efficiency. J Anim Sci 76: 2354-2367, 1998. 24. Gregoire FM, Smas CM, and Sul HS. Understanding adipocyte differentiation. Physiol Rev 78: 783-809, 1998. 25. Grosfeld A, Andre J, Hauguel-De Mouzon S, Berra E, Pouyssegur J, and Guerre-Millo M. Hypoxia-inducible factor 1 transactivates the human leptin gene promoter. J Biol Chem 277: 42953-42957, 2002. 26. He Y, Chen H, Quon MJ, and Reitman M. The mouse obese gene. Genomic organization, promoter activity, and activation by CCAAT/enhancer-binding protein alpha. M, Yoshimasa Y, Nishi S, and et al. Structural organization and chromosomal assignment of the human obese gene. 33. Jaquet D, Gaboriau A, Czernichow P, and Levy-Marchal C. Insulin resistance early in adulthood in subjects born with intrauterine growth retardation. J Clin Endocrinol Metab 85: 1401-1406, 2000. 34. Jaquet D, Gaboriau A, Czernichow P, and Levy-Marchal C. Relatively low serum leptin levels in adults born with intra-uterine growth retardation. International Journal of Obesity & Related Metabolic Disorders 25: 491, 2001. 35. Jaquet D, Leger J, Levy-Marchal C, Oury JF, and Czernichow P. Ontogeny of leptin in human fetuses and newborns: effect of intrauterine growth retardation on serum leptin concentrations. 20 36. Jaquet D, Leger J, Tabone MD, Czernichow P, and Levy-Marchal C. High serum leptin concentrations during catch-up growth of children born with intrauterine growth retardation. J Clin Endocrinol Metab 84: 1949-1953, 1999. 37. Kauter K, Ball M, Kearney P, Tellam R, and McFarlane JR. Adrenaline, insulin and glucagon do not have acute effects on plasma leptin levels in the sheep: development and characterisation of an ovine leptin ELISA. J Endocrinol 166: 127-135, 2000. 38. Kind KL, Owens JA, Robinson JS, Quinn KJ, Grant PA, Walton PE, Gilmour RS, and Owens PC. Effect of restriction of placental growth on expression of IGFs in fetal sheep: relationship to fetal growth, circulating IGFs and binding proteins. J Endocrinol 146: 23-34, 1995. 39. Lau D, Shillabeer G, Wong K, Tough S, and Russell J. Influence of paracrine factors on preadipocyte replication and differentiation. Int J Obes Relat Metab Disord 14: 193-201, 1990. 40. Law CM, Barker DJ, Osmond C, Fall CH, and Simmonds SJ. Early growth and abdominal fatness in adult life. J Epidemiol Community Health 46: 184-186, 1992. 41. Leger J, Levy-Marchal C, Bloch J, Pinet A, Chevenne D, Porquet D, Collin D, and Czernichow P. Reduced final height and indications for insulin resistance in 20 year olds born small for gestational age: regional cohort study. BMJ 315: 341-347, 1997. 42. LeRoith D, Werner H, Beitner-Johnson D, and Roberts CT, Jr. Molecular and cellular aspects of the insulin-like growth factor I receptor. Endocr Rev 16: 143-163, 1995. 43. Levy-Marchal C, Jaquet D, and Czernichow P. Long-term metabolic consequences of being born small for gestational age. Semin Neonatol 9: 67-74, 2004. 44. Lithell HO, McKeigue PM, Berglund L, Mohsen R, Lithell UB, and Leon DA.
Reproduction in Domestic Animals, 2011
Iberian pig is the most abundant Mediterranean swine. The lack of knowledge of the reproductive physiology of Mediterranean genotypes, with predisposition to obesity, led us to evaluate the influence of body condition and metabolic status at weaning on the resumption of follicular growth and the appearance of post-weaning oestrus. Females failing to display post-weaning oestrus showed a high decrease in backfat mass during lactation; backfat depth at weaning was therefore lower than in sows becoming in oestrus. Females not bearing oestrus behaviour showed lower plasma leptin levels and higher ghrelin concentrations at weaning. Moreover, these sows evidenced dyslipidemic profile (increased triglyceridemia and cholesterolemia) and mobilization of fat reserves. Hence, changes in metabolic regulation of Iberian pigs may originate large effects on the resumption of ovulatory activity after weaning.