86
certain possible association has been developed. Such as, lack of sleep is associated with chronic activation of sympathetic nervous system, and direct sympathetic innervations to adipose tissues promotes stimulation of lipolysis, giving rise
to elevated free fatty acids [23]. Additionally, studies have also indicated that
chronic stress and sleep deprivation are responsible for initiation and progression
of metabolic disorders involving obesity. This mechanism is related to the alteration in neuroendocrine response and hyperactivation of hypothalamic-pituitaryadrenal axis [24]. Admittedly, sleep loss is associated with low leptin and increased
ghrelin, leading towards more hunger and ultimately obesity [25]. Meanwhile,
in vitro studies have also indicated that hypoxia mainly obstructs lipoprotein lipase
activity in differentiated individually preadipocytes. Yet, in vivo studies demonstrate elevated postprandial non-esterified fatty acids (NEFA), during small sessions involving intermitted hypoxia [26]. It is obvious that improving sleep hobbits
via sleep as well as treating sleep disorders along with other radical nutritional
interventions can be best therapeutic approach in prophylaxis of metabolic disorders [24].
Non-Alcoholic Fatty Liver Disease
NAFLD signifies the presence of macrovascular alteration in the absence of considerable alcoholic use without any inflammation (stenosis) and lobular inflammation.
It is categorized into two subgroups; one is non-alcoholic fatty liver (NAFL) and
other is non-alcoholic steatohepatitis (NASH). Likewise, NASH is defined with
existence of hepatic steatosis as well as inflammation along with hepatic injury [27].
While on the other hand, NAFLD is defined with liver manifestation, accompanied
by radiographic and histologic evidence for the presence of fat deposition in liver,
may or may not be linked with inflammation [28].
NAFLD is generally affiliated with metabolic syndrome, hyperlipidemia, diabetes, and obesity. Generally, approximately 80% of patients having metabolic syndromes also possess NAFLD [27]. Unlike most other disorders, NAFLD do not
follow sequenced/organized progression, means a person may be prone to fibrosis
without developing NASH stage, or may be exposed to liver cancer without having
fibrosis or histologic NASH [29]. In fact, the main disturbance in lipid metabolism
during NAFLD is due to elevated de novo lipogenesis and hepatic uptake, which is
accompanied with insufficient rise in compensatory fatty acid oxidation (Fig. 5.1).
This give rise to increase in cellular damage and further aids disease progression by
triggering oxidative stress, particularly with the raised oxidation in cytochromes
and also in peroxisomes, along with mitochondrial dysfunction [30]. Alternatively,
the exact molecular mechanism concerned with fat deposition in liver is not completely understood. Yet, compromised mitochondrial function, adipose tissue
inflammation, lipotoxicity, oxidative stress, insulin resistance, and endoplasmic
reticulum stress play a critical role [31]. Actually, during normal physiological process, substrate supply and oxidation including secretion tightly control the lipid
K. Haider et al.
certain possible association has been developed. Such as, lack of sleep is associated with chronic activation of sympathetic nervous system, and direct sympathetic innervations to adipose tissues promotes stimulation of lipolysis, giving rise
to elevated free fatty acids [23]. Additionally, studies have also indicated that
chronic stress and sleep deprivation are responsible for initiation and progression
of metabolic disorders involving obesity. This mechanism is related to the alteration in neuroendocrine response and hyperactivation of hypothalamic-pituitaryadrenal axis [24]. Admittedly, sleep loss is associated with low leptin and increased
ghrelin, leading towards more hunger and ultimately obesity [25]. Meanwhile,
in vitro studies have also indicated that hypoxia mainly obstructs lipoprotein lipase
activity in differentiated individually preadipocytes. Yet, in vivo studies demonstrate elevated postprandial non-esterified fatty acids (NEFA), during small sessions involving intermitted hypoxia [26]. It is obvious that improving sleep hobbits
via sleep as well as treating sleep disorders along with other radical nutritional
interventions can be best therapeutic approach in prophylaxis of metabolic disorders [24].
Non-Alcoholic Fatty Liver Disease
NAFLD signifies the presence of macrovascular alteration in the absence of considerable alcoholic use without any inflammation (stenosis) and lobular inflammation.
It is categorized into two subgroups; one is non-alcoholic fatty liver (NAFL) and
other is non-alcoholic steatohepatitis (NASH). Likewise, NASH is defined with
existence of hepatic steatosis as well as inflammation along with hepatic injury [27].
While on the other hand, NAFLD is defined with liver manifestation, accompanied
by radiographic and histologic evidence for the presence of fat deposition in liver,
may or may not be linked with inflammation [28].
NAFLD is generally affiliated with metabolic syndrome, hyperlipidemia, diabetes, and obesity. Generally, approximately 80% of patients having metabolic syndromes also possess NAFLD [27]. Unlike most other disorders, NAFLD do not
follow sequenced/organized progression, means a person may be prone to fibrosis
without developing NASH stage, or may be exposed to liver cancer without having
fibrosis or histologic NASH [29]. In fact, the main disturbance in lipid metabolism
during NAFLD is due to elevated de novo lipogenesis and hepatic uptake, which is
accompanied with insufficient rise in compensatory fatty acid oxidation (Fig. 5.1).
This give rise to increase in cellular damage and further aids disease progression by
triggering oxidative stress, particularly with the raised oxidation in cytochromes
and also in peroxisomes, along with mitochondrial dysfunction [30]. Alternatively,
the exact molecular mechanism concerned with fat deposition in liver is not completely understood. Yet, compromised mitochondrial function, adipose tissue
inflammation, lipotoxicity, oxidative stress, insulin resistance, and endoplasmic
reticulum stress play a critical role [31]. Actually, during normal physiological process, substrate supply and oxidation including secretion tightly control the lipid
K. Haider et al.