Day‐restricted feeding during pregnancy and lactation programs glucose intolerance and impaired insulin secretion in male rat offspring

The maternal environment during pregnancy and lactation plays a determining role in programming energy metabolism in offspring. Among a myriad of maternal factors, disruptions in the light/dark cycle during pregnancy can program glucose intolerance in offspring. Out‐of‐phase feeding has recently been reported to influence metabolism in adult humans and rodents; however, it is not known whether this environmental factor impacts offspring metabolism when applied during pregnancy and lactation. This study aims to determine whether maternal day‐restricted feeding (DF) influences energy metabolism in offspring.

[1]  P. Persson Good publication practice in physiology 2015 , 2015, Acta physiologica.

[2]  L. Pulakat,et al.  Regulation of Cardiac Expression of the Diabetic Marker MicroRNA miR-29 , 2014, PloS one.

[3]  J. Antignac,et al.  Time window-dependent effect of perinatal maternal protein restriction on insulin sensitivity and energy substrate oxidation in adult male offspring. , 2014, American journal of physiology. Regulatory, integrative and comparative physiology.

[4]  D. Kennaway,et al.  Metabolic consequences of timed feeding in mice , 2014, Physiology & Behavior.

[5]  D. Hazlerigg,et al.  Gestational Chronodisruption Impairs Hippocampal Expression of NMDA Receptor Subunits Grin1b/Grin3a and Spatial Memory in the Adult Offspring , 2014, PloS one.

[6]  P. Sethupathy,et al.  Beta Cell 5′-Shifted isomiRs Are Candidate Regulatory Hubs in Type 2 Diabetes , 2013, PloS one.

[7]  R. Buijs,et al.  Shift Work or Food Intake during the Rest Phase Promotes Metabolic Disruption and Desynchrony of Liver Genes in Male Rats , 2013, PloS one.

[8]  D. Kennaway,et al.  Characterisation of the Maternal Response to Chronic Phase Shifts during Gestation in the Rat: Implications for Fetal Metabolic Programming , 2013, PloS one.

[9]  L. Dalgaard,et al.  Syntaxin-1a is a Direct Target of miR-29a in Insulin-producing β-Cells , 2013, Hormone and Metabolic Research.

[10]  T. Moran,et al.  Maternal High-Fat Diet During Gestation or Suckling Differentially Affects Offspring Leptin Sensitivity and Obesity , 2012, Diabetes.

[11]  J Abbott,et al.  Night eating syndrome: implications for severe obesity , 2012, Nutrition & Diabetes.

[12]  J. Cipolla-Neto,et al.  Maternal Melatonin Programs the Daily Pattern of Energy Metabolism in Adult Offspring , 2012, PloS one.

[13]  B. Portha,et al.  Early-Life Origins of Type 2 Diabetes: Fetal Programming of the Beta-Cell Mass , 2011, Experimental diabetes research.

[14]  J. Long,et al.  MicroRNA-29c Is a Signature MicroRNA under High Glucose Conditions That Targets Sprouty Homolog 1, and Its in Vivo Knockdown Prevents Progression of Diabetic Nephropathy* , 2011, The Journal of Biological Chemistry.

[15]  R. Buijs,et al.  Food intake during the normal activity phase prevents obesity and circadian desynchrony in a rat model of night work. , 2010, Endocrinology.

[16]  P. Meda,et al.  Involvement of MicroRNAs in the Cytotoxic Effects Exerted by Proinflammatory Cytokines on Pancreatic β-Cells , 2010, Diabetes.

[17]  F. Turek,et al.  Circadian Timing of Food Intake Contributes to Weight Gain , 2009, Obesity.

[18]  M. Morris,et al.  Maternal and postnatal overnutrition differentially impact appetite regulators and fuel metabolism. , 2008, Endocrinology.

[19]  A. Boschero,et al.  Signal transducer and activator of transcription 3-regulated sarcoendoplasmic reticulum Ca2+-ATPase 2 expression by prolactin and glucocorticoids is involved in the adaptation of insulin secretory response during the peripartum period. , 2007, The Journal of endocrinology.

[20]  Y. Leung,et al.  SNAREing Voltage-Gated K+ and ATP-Sensitive K+ Channels: Tuning β-Cell Excitability with Syntaxin-1A and Other Exocytotic Proteins. , 2007, Endocrine reviews.

[21]  S. Ozanne,et al.  Experimental IUGR and later diabetes , 2007, Journal of internal medicine.

[22]  F. Pattou,et al.  Glucotoxicity inhibits late steps of insulin exocytosis. , 2007, Endocrinology.

[23]  B. V. van Bon,et al.  Programming of glucose-insulin metabolism in adult sheep after maternal undernutrition. , 2005, American journal of physiology. Regulatory, integrative and comparative physiology.

[24]  J. Seckl,et al.  Glucocorticoid exposure in late gestation in the rat permanently programs gender-specific differences in adult cardiovascular and metabolic physiology. , 2004, American journal of physiology. Endocrinology and metabolism.

[25]  S. Ozanne,et al.  Early growth restriction leads to down regulation of protein kinase C zeta and insulin resistance in skeletal muscle. , 2003, The Journal of endocrinology.

[26]  B. Selmaoui,et al.  Food access schedule and diet composition alter rhythmicity of serum melatonin and pineal NAT activity , 2001, Physiology & Behavior.

[27]  S. Nagamatsu,et al.  Decreased expression of t-SNARE, syntaxin 1, and SNAP-25 in pancreatic beta-cells is involved in impaired insulin secretion from diabetic GK rat islets: restoration of decreased t-SNARE proteins improves impaired insulin secretion. , 1999, Diabetes.

[28]  P. Czernichow,et al.  Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat , 1998, Diabetologia.

[29]  M. Nyirenda,et al.  Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring. , 1998, The Journal of clinical investigation.

[30]  M. Shipston,et al.  Attenuated neuroendocrine responses to emotional and physical stressors in pregnant rats involve adenohypophysial changes , 1998, The Journal of physiology.

[31]  P. Pévet,et al.  Phase-Advanced Daily Rhythms of Melatonin, Body Temperature, and Locomotor Activity in Food-Restricted Rats Fed during Daytime , 1997, Journal of biological rhythms.

[32]  C. Hales,et al.  Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis , 1992, Diabetologia.

[33]  J. Neel Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"? , 1962, American journal of human genetics.

[34]  P. Tsao,et al.  MicroRNA-29b regulation of abdominal aortic aneurysm development. , 2014, Trends in cardiovascular medicine.

[35]  L. Velloso,et al.  Long-term disruption of maternal glucose homeostasis induced by prenatal glucocorticoid treatment correlates with miR-29 upregulation. , 2014, American journal of physiology. Endocrinology and metabolism.

[36]  W. Lee,et al.  Glucose intolerance and lipid metabolic adaptations in response to intrauterine and postnatal calorie restriction in male adult rats. , 2013, Endocrinology.

[37]  L. Caperuto,et al.  UPR induces transient burst of apoptosis in islets of early lactating rats through reduced AKT phosphorylation via ATF4/CHOP stimulation of TRB3 expression. , 2011, American journal of physiology. Regulatory, integrative and comparative physiology.

[38]  Y. Leung,et al.  SNAREing voltage-gated K+ and ATP-sensitive K+ channels: tuning beta-cell excitability with syntaxin-1A and other exocytotic proteins. , 2007, Endocrine reviews.

[39]  P. Clifton,et al.  Effect of maternal feed restriction during pregnancy on glucose tolerance in the adult guinea pig. , 2003, American journal of physiology. Regulatory, integrative and comparative physiology.