Offspring of obese mice display enhanced intake and sensitivity for palatable stimuli, with altered expression of taste signaling elements

Abstract

Maternal body mass index and gestational weight gain predict future obesity status of the offspring. In studies of both rodents and non-human primates, maternal obesity also predicts a preference for palatable foods in the offspring. In this study, we used C57BL/6J mice to investigate whether an underlying cause for an increase in palatable food consumption in the offspring of obese mice was a change in taste function. Adult female mice were fed a normal chow (NC) or a high fat diet (HFD) for 5 weeks before mating, then also during the gestation (3 weeks) and lactation (3 weeks) periods, with offspring always maintained on a normal chow diet; thus the only experience offspring had with high fat food was via maternal exposure. Offspring exhibited similar weight, blood glucose levels and baseline water and chow intake in adulthood. Taste response was assessed after reaching maturity, using brief-access taste testing, with female offspring of obese dams showing an enhanced response to sucrose, and both sexes consuming more sucrose, sucralose and high fat diet if from obese mothers. Offspring also exhibited increased taste bud expression of mRNA for sweet receptor subunits T1R (Taste receptor type) 2 and 3, as well as other markers associated with taste signaling. Taste morphology in both groups appeared similar. Results indicate that obesity in the mother may lead to unhealthy feeding behavior in the offspring, correlating with altered expression of taste signaling elements, which likely drive increased avidity for palatable foods. Obesity and metabolic programming. Obesity is a chronic worldwide health issue with profound associated healthcare implications. Obesity is increasing at a higher rate in women than men 1 , and is also increasing in children 2. In the United States, half women of childbearing age are overweight or obese 3. Maternal obesity puts a child at increased risk for both childhood and adulthood obesity 4 , thus future generations may be at risk for obesity even before birth. Events occurring in utero can have long-term influences on disease risk later in life, termed 'early life programming' , or the fetal origins hypothesis 5,6. Maternal obesity and over-nutrition are now recognized as programming factors, leading to permanent changes in offspring metabolism, behavior, and appetite regulation, and a propensity for developing obesity, metabolic, and behavioral problems 7-9. Recently, links have been uncovered between obesity and the taste system, with studies in mice 10,11 and humans 11,12 suggesting weight gain may influence the taste system. Maternal adiposity predisposes offspring to diet-induced obesity. Rodent studies of maternal obesity demonstrate that the offspring, when challenged with HFD after weaning, are predisposed to weight gain, poor glycemic control, and metabolic dysregulation 13,14. This propensity for diet-induced obesity in the

Histopathology of the kidney and seroprevalence of leptospirosis in wild rats in Baghdad Province, Iraq

“…The use of age groups in this study conforms to the study by Choo et al [34]. Despite that the number of males and females was equal (Table-1), considering the distribution of age groups, the juvenile group composed of significantly the largest number of rats.…”

“…Despite that the number of males and females was equal (Table-1), considering the distribution of age groups, the juvenile group composed of significantly the largest number of rats. This might be explained by the fact that juvenile rats are not experts in collecting their food and look at the surroundings differently from the adult rats [34].…”

Genetic Polymorphism of GABRG2 rs211037 is Associated with Drug Response and Adverse Drug Reactions to Valproic Acid in Chinese Southern Children with Epilepsy

“…[38][39][40] A study in mice suggested that changes in taste signaling taste signaling pathways could trigger changes in appetite, which -might lead to obesity. 41,42 Evidence revealed that the sensitivity of GABA played a crucial role in determining fat depotselective adipose tissue macrophage infiltration in obesity. 43 GABA receptor binding was found to modulate obesity and prioritizing a high-fat diet.…”

The Influence of Common Noncommunicable Diseases on Chemosensory Perception and Clinical Implications in Children and Adolescents

“…Various psychophysical studies reported that adults with obesity have an altered taste/oro-sensory system [e.g., 48 -52]. Some recent studies performed in animal models and on adults with obesity [53][54][55][56], linked these differences in chemosensory perception to the expression of several inflammatory markers in the fungiform taste buds, alongside a downregulation in transcription of classical taste markers responsible for regulating several taste sensations in obese. However, evidence is lacking in children and adolescents with obesity and taste perception in this target group has been greatly evaluated through the bitter responsiveness to the 6-n-propylthiuracil (PROP) compound.…”