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a drastic drop in body temperature right before death. Furthermore, skin
ulcerations developed on the footpads of the animals in addition to an overall
unkempt appearance. During the SD period, there were no stress symptoms
such as stress ulcers, increased corticosterone levels or decreased metabolic rate
indicating that SD produces distinct detrimental effects on homeostasis
compared to those of stress related hypothalamic-pituitary-adrenal activation
(Rechtschaffen et al 1983).
However, during these SD experiments a rather intriguing finding emerged
that seemed to tie in with the reciprocal relationship between mammalian sleep
and energy homeostasis. There was a paradoxical decrease in weight with the
increased food intake indicating that food derived energy was being utilized in
a non-thermogenic capacity. This negative energy balance could be the result
of decreases in key metabolic hormones (e.g. insulin) (Everson and Crowley
2004) or increased activity in hypothalamic feeding centers (Koban et al 2006)
or increases in brown adipose tissue thermogenesis in animals. Yet, this
catabolic effect of SD seems to only appear in small mammals thus far while
human findings remain inconclusive. With that said, several epidemiological
studies have suggested a link between short sleep duration and increased
obesity or adiposity (Penev 2007). This supports other studies showing that
short sleep periods can influence the neuroendocrine control of energy balance
by altering levels of leptin and ghrelin, two hormones involved in energy
metabolism, in a way that promotes feeding in the absence of increased caloric
need, which could eventually lead to weight gain. Shorter sleep has been
suggested to alter glucose metabolism and result in diabetic complications such
as insulin resistance in healthy young adults (Gottlieb et al 2005). This
metabolic derangement could be due to increased circulation of counter-
regulatory catabolic and anabolic hormones (e.g. cortisol and growth
hormone) (Yaggi et al 2006) or even elevated secretion of both pro- and
anti-inflammatory cytokines (e.g. tumor necrosis factor and interleukin-6)
(Vgontzas et al 2006). Thus, the finding that SD leads to increased energy
expenditure and weight loss is consistent with the role of sleep in energy
conservation possibly explaining its role as a risk factor for metabolic disorders
such as diabetes mellitus and obesity.
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16.4.1 Sleep Disruption and Neural Function
Both partial and total SD experiments play key roles in elucidating many of
the effects that sleep exerts on memory consolidation (Smith and Rose 1996).
In other words, as synaptic plasticity is thought to underlie memory formation,
blocking the consolidation that occurs during these sleep stages using SD
models reveals certain impairments. Sleep deprivation studies are generally
divided in to partial SD, which is defined as one night of reduced or
fragmented sleep and total SD, which involves no sleep during a normal sleep-
wake cycle. For example, the disc-on-water method can be considered forms of
chronic total SD (Rechtschaffen et al 1983) whereas other, less stressful
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