Metabolic Consequence of Short Term Starvation in Gastrointestinal Diseases: A Mini Review
Authored by Mayadhar Barik
Abstract
The metabolic consequences of preoperative starvation
and carbohydrate loading and mechanisms linking insulin resistance to
impaired mitochondrial function are discussed. We just find out the
short-term energy deprivation combinations with the health control
subject. Followed by the nutrition and metabolism on molecular basis of
per operative surgery. Majority of animal studies have shown that
short-term energy deprivation decreases mitochondrial ATP synthesis
capacity and complex activity, and increases oxidative injury which lead
to development of insulin resistance (IR) during starvation and
associated with an impaired mitochondrial function. From animal to human
subject we thoroughly find out that short-term starvation (STS) causes
mitochondrial dysfunction and it underlies the development of insulin
resistance (IR) in patients undergoing elective surgery (ES).
Keywords: Digestive tract; Histology; Ontogenetic development; StarvationIntroduction
Effects of starvation were mainly evident on the
degeneration of cells in digestive organs as seen in the shrinkage and
separation of cells [1].
The loss of intercellular substances in the liver, pancreas, intestine
and stomach changes became more severe with increased duration of
starvation. In addition, the histological structure of the digestive
tracts of starved larvae and juveniles partly recovered after
re-feeding, and the effects of starvation on miiuy croaker were age
dependent [2].
Material and Methods
We just find out the short-term energy deprivation
combinations with the health control subject. Followed by the nutrition
and metabolism on molecular basis of per operative surgery. In a mean
while we justify that these statement as per our twenty years of the
research experience.
Results and Discussion
The combined treatment profoundly impairs cancer
glucose metabolism and virtually abolishes lesion growth in experimental
models of breast and colon carcinoma suggest that energy metabolism
(EM) is more promising target to reduce cancer progression [3].
However, short term starvation is the medical condition of congenital
hypertrophic pyloric stenosis. Starvation resulting in reduction of more
than 15% of the expected body weight in infancy was associated with
poorer learning abilities, especially those involving short-term memory
and attention [4].
As a total parenteral nutrition prevents patients with short bowel
syndrome from dying of starvation, having short bowel remains a severely
debilitating condition, this therapy is associated with significant
morbidity and patients suffer from consequences of long-term
immunosuppression. Now new frontier in medicine in the field of tissue
engineering used an autologous tissue as a patch to study intestinal
regeneration by consists of seeding a resorbable scaffold and
implanting. Researcher construct the regeneration of neointestine is
able to creation of esophagus, stomach, small bowel and colon has been
demonstrated. We suggest that tissue-engineered intestine become a real
therapeutic option in the not too distant future for patients having
inadequate intestinal tissue [4].
An Ulcerative colitis be classified as a nutritional
colitis in that colonic epithelial cells are unable to utilize SCFAs
reflecting epithelial starvation despite abundant SCFAs. Additionally,
increased succinate/Complex II-dependent O [2]
consumption and elevated oxidative stress (OS) and apoptosis indicated
that the glucose and amino acid deficiency conditions imposed through
the STS promote an anti-Warburg effect. It increased oxygen consumption
but failure to generate ATP and resulting in oxidative damage and
apoptosis [5].
The model of animal to human subject we thoroughly find out that
short-term starvation (STS) causes mitochondrial dysfunction and it
underlies the development of insulin resistance (IR) in patients who
undergoing elective surgery (ES) As well.
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