Abstract:
Obesity is the result of genetics which predisposes an individual to obesity and
environmental factors, resulting in excessive weight gain. A well-established linear relationship
exists between hypertension and obesity. The combined burden of hypertension and
obesity poses significant health and economic challenges. Many environmental factors and
genetic traits interact to contribute to obesity-linked hypertension. These include excess
sodium re-absorption or secretion by the kidneys, a hypertensive shift of renal-pressure
and activation of the sympathetic nervous system. Most individuals suffering from hypertension
need drugs in order to treat their raised blood pressure, and while a number of
antihypertensive therapeutic agents are currently available, 50% of cases remain uncontrolled.
In order to develop new and effective therapeutic agents combating obesity-induced
hypertension, a thorough understanding of the molecular events leading to adipogenesis is
critical. With the advent of whole genome and exome sequencing techniques, new genes and
variants which can be used as markers for obesity and hypertension are being identified. This
review examines the role played by alternative splicing (AS) as a contributing factor to the
metabolic regulation of obesity-induced hypertension. Splicing mutations constitute at least
14% of the disease-causing mutations, thus implicating polymorphisms that effect splicing as
indicators of disease susceptibility. The unique transcripts resulting from the alternate
splicing of mRNA encoding proteins that play a key role in contributing to obesity would
be vital to gain a proper understanding of the genetic causes of obesity. A greater knowledge
of the genetic basis for obesity-linked hypertension will assist in the development of
appropriate diagnostic tests as well as the identification of new personalized therapeutic
targets against obesity-induced hypertension.
