The present study aimed to determine the effect of a high fructose
diet on brown adipose tissue development in aging congenic obese T2DM rats. The
physiological merits of brown adipose tissue (BAT) metabolism as an efficient
potential energy buffer that when deficient, may be a contributor to excess fat
accretion and to the development of obesity in man and animals. As such, it offers to be a potential target
for therapies that could be developed for its treatment. To determine the
effects of dietary fructose consumption on development and cellularity of brown
adipose tissue in T2DM, groups of lean and obese SHR/Ntul//-cp rats
demonstrating insulin resistance (IR) and heritable T2DM were fed diets
containing 54% (w/w) carbohydrate as cornstarch (CS diet) or equal parts CS
plus fructose (CSF diet) plus essential proteins, fats, vitamins, minerals, and
dietary fiber from one to nine months of age.
The SHR/Ntul//-cp rat is a congenic animal model in which the only
genetic difference between the phenotypes is the epigenetic inheritance and
natural expression of the obese (-cp) trait, which is distinct from dietary,
toxicologic, or pharmacologic factors and is accompanied by the development of
chronic insulin resistance (IR) and non-insulin-dependent diabetes (T2DM)
shortly after weaning in the obese phenotype.
The effects of this study indicate that final weight gain and
Interscapular brown adipose tissue mass and cellularity are significantly
greater in the obese than in the lean phenotype. In addition, the effects of a
high fructose diet resulted in only modest increases in body weight gain, and
in differential effects on IBAT cellularity and cell lipid content. Weight gain
of obese >> lean and was greater when fed the CSF than the CS diet in
both phenotypes; Interscapular brown adipose tissue (IBAT) mass of obese
>> Lean and was similar in both phenotypes. IBAT Mass: Body weight of Obese >>
lean, and trended greater in lean CSF vs CS but less in Obese CSF vs CS. IBAT
cell size and lipid content of obese >> lean, and the CS vs CSF diet was
similar in lean but decreased in the obese phenotype. IBAT cell number of obese
>>> lean, while IBAT cell number of lean CSF > lean CS, but IBAT
cell number of obese was similar with both diets. Lipoprotein lipase activity (LPL) of lean >>
obese and trended to be greater with the CSF than the CS diet in both
phenotypes and IBAT tissue lipid content of obese >> lean with a trend
toward CSF > CS in both phenotypes. These results indicate that IBAT
development occurs via hyperplasia and hypertrophy in the Obese phenotype of
this strain and that long term consumption of the high Fructose diet enhances
IBAT cellularity in the lean phenotype while the IBAT cellularity was maximally
enhanced by both diets in the obese phenotype.
These results further indicate that the impact of long-term
consumption of a high fructose diet throughout much of the natural lifespan
impacts the development of IBAT mass and cellularity differentially in the lean
and obese+T2DM phenotype, likely at least in part due to contributions of
longstanding IR in the obese+T2DM animals. Because IR is known to impede
cellular glucose uptake in isolated brown adipocytes as an essential process in
the expression of cellular thermogenic responses, any potential mechanisms to
override or bypass the process or decrease the magnitude of IR would be
presumed to exert a beneficial effect. Fructose may increase the potential for
the expression of IBAT development and the expression of non-shivering
thermogenesis in response to changes in food and environment because it can
enter tissues independently of insulin activities, for example, through the
GLUT1 and GLUT5 transporters. Nevertheless, in the current investigation, it
was discovered that overall fructose consumption was neither significantly
advantageous nor ameliorative in resolving crucial parameters of brown adipose
tissue expression as contributors to the development of obesity in the
obese+T2DM phenotype.
Author
(s) Details
Orien L
Tulp
Colleges of Medicine and Graduate Studies, University of Science
Arts and Technology, Montserrat, BWI MSR1110 and Einstein Medical Institute, N.
Palm Beach, FL, 33408, USA.
Please see the book here:- https://doi.org/10.9734/bpi/crpbs/v2/2210
