Photoperiod Regulates Lean Mass Accretion, but Not Adiposity, in Growing F344 Rats Fed a High Fat Diet

Abstract

In this study the effects of photoperiod and diet, and their interaction, were examined for their effects on growth and body composition in juvenile F344 rats over a 4-week period. On long (16L:8D), relative to short (8L:16D), photoperiod food intake and growth rate were increased, but percentage adiposity remained constant (ca 3-4%). On a high fat diet (HFD), containing 22.8% fat (45% energy as fat), food intake was reduced, but energy intake increased on both photoperiods. This led to a small increase in adiposity (up to 10%) without overt change in body weight. These changes were also reflected in plasma leptin and lipid levels. Importantly while both lean and adipose tissue were strongly regulated by photoperiod on a chow diet, this regulation was lost for adipose, but not lean tissue, on HFD. This implies that a primary effect of photoperiod is the regulation of growth and lean mass accretion. Consistent with this both hypothalamic GHRH gene expression and serum IGF-1 levels were photoperiod dependent. As for other animals and humans, there was evidence of central hyposomatotropism in response to obesity, as GHRH gene expression was suppressed by the HFD. Gene expression of hypothalamic AgRP and CRH, but not NPY nor POMC, accorded with the energy balance status on long and short photoperiod. However, there was a general dissociation between plasma leptin levels and expression of these hypothalamic energy balance genes. Similarly there was no interaction between the HFD and photoperiod at the level of the genes involved in thyroid hormone metabolism (Dio2, Dio3, TSHβ or NMU), which are important mediators of the photoperiodic response. These data suggest that photoperiod and HFD influence body weight and body composition through independent mechanisms but in each case the role of the hypothalamic energy balance genes is not predictable based on their known function.

Identification of mutations through dominant screening for obesity using C57BL/6 substrains

“…Unlike obesity in Sim1 or Mc4r mutant mice, the obesity induced in the high-fat diet rodent model is relevant to human obesity which is strongly associated with the recent availability of high-calorie food. Prolonged high-fat diet feeding promotes leptin-resistance18 and alters hypothalamic gene expression patterns, such as decreased Agrp and Ghrh mRNA levels without significant change in Pomc mRNA level41495051, which is consistent with the current results for DIO mice. Common changes between DIO mice and genetically obese mice, such as decreased Agrp and Avp mRNA levels, might be secondary to obesity-associated changes, including increased leptin and insulin levels and polyuria52.…”

A unifying hypothesis for control of body weight and reproduction in seasonally breeding mammals

“…Agouti-related peptide (AgRP) neurones, which co-express neuropeptide Y (NPY), are a key cluster of neurones, which increase food intake and body weight when activated. 23,79,80 These findings highlight how the tanycytes are an important route in the regulation of the activity of the AgRP/NPY and POMC neurones. 77 They are regulated by leptin, which is taken up through the fenestrated capillaries of the median eminence and is delivered to the arcuate nucleus via the tanycytes.…”

“…In mammals, melatonin acts through melatonin receptors located on the PT cells to regulate TSH (α-and β-subunit gene and protein expression). [22][23][24] It has been inferred that TSH acts in a paracrine manner to activate TSH receptors located in specialised glial cells, the tanycytes, around the third ventricle of the hypothalamus. 17 Additionally, the effects of a short photoperiod on TSH immunoreactivity in the PT were mimicked by melatonin injections in hamsters held under long days.…”

Prss56 expression in the rodent hypothalamus: Inverse correlation with pro‐opiomelanocortin suggests oscillatory gene expression in adult rat tanycytes

“…Pro‐opiomelanocortin (POMC) is a critically important regulatory protein acting both as a hormonal and a neurotransmitter precursor: adrenocorticotropin (ACTH) released from pituitary corticotrophs regulates corticosteroid production of the adrenal gland, while α‐melanocyte‐stimulating hormone (α‐MSH) released from hypothalamic neurons regulates food intake and energy expenditure (Cawley, Li, & Loh, ). In rats, Pomc is also expressed in hypothalamic tanycytes (Baubet et al, ; Larsen & Mau, ; Lu et al, ; Ross et al, ; Sergeyev, Vegeyeva, & Akmayev, ; Willesen, Kristensen, & Romer, ; Wittmann et al, ), ependymoglial cells that reside in the ventrolateral wall and floor of the caudal third ventricle, and also within the median eminence and infundibular stalk (Wittkowski, ; Wittmann et al, ). The function of POMC in tanycytes is not yet understood.…”