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Global Translational Medicine                                                 Brain morphology in obesity



              The problem of obesity is now being considered not only   Changes in the cerebral cortex, which is responsible for
            in terms of its damage to somatic health but also its negative   the cognitive control of food intake, may either contribute
            effects  on  psycho-emotional  status,  cognitive  abilities,   to or result from obesity, further supporting the notion of
            and behavior.  Experiments in rats have shown that long-  impaired regulation of eating behavior.
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            term diet-induced obesity, initiated in prepubertal age,   The study aimed to investigate the histological
            leads to depression and neuroinflammation. A review of   characteristics of the PFC and hippocampus in male and
            the current literature generally confirms the link between   female rats subjected to diet-induced visceral obesity.
            obesity  and  depression  in  humans,  although  there  are
            conflicting findings in some studies. 5            2. Materials and methods
              Experimental studies in rats also show that high-fat   2.1. Animals and diets
            or combined high-fat and sucrose diets cause cognitive
            impairments, particularly in reduced short-term and   The study was conducted on 2-month-old sexually mature
            visuospatial memories.  Early obesity, before the onset   male and female Wistar rats. These rats were bred in-house
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            of diabetes or metabolic syndrome, leads to cognitive   in a certified vivarium at the Institute of Physiology of the
            impairment. This is due to changes in the PFC, including   National Academy of Sciences of Belarus. They were kept
            synapse loss, a reduction in dendritic spine density, altered   under a 12/12  h light/dark cycle at a temperature of 22
            expression of synaptic proteins, and structural changes in   ± 2°C and humidity of 60 – 65%. The male (n = 27) and
            microglia. The results strongly suggest that obesity can be   female (n = 27) Wistar rats were randomly divided into
            considered a contributing factor to dysfunction of the PFC. 7  two experimental groups: control and HCD. The control
                                                               group, consisting of 13 male and 14 female rats, received
              There is emerging evidence of a link between obesity   the standard diet (StD), while the HCD group, comprising
            and brain development during ontogenesis. For example,   14 male and 13 female rats, was given an HCD for 16 weeks.
            Laurent  et al.  examined  the relationship  between  body
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            mass index (BMI), cortical thickness, and executive   The HCD consisted of StD supplemented with animal
            function in children. Among the 3190 children studied   fats (lard) (45% of daily caloric content) and a 10% fructose
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            (mean age 10.0 years; 51.0% boys), those with a higher-  solution (replacing water) ad libitum.  The caloric content
            than-normal BMI showed reduced cortical thickness.   of StD for each rat was 150 kcal/day (i.e., the normal diet at
                    9
            Hall  et al.  suggested that the thickness of the inferior   the vivarium of the Institute of Physiology of the National
            frontal gyrus and lateral orbitofrontal cortex may serve   Academy of Sciences of Belarus). In contrast, the caloric
            as predictors of body composition. The study concluded   content of HCD for each rat was 228 kcal/day.
            that PFC morphology is a reliable predictor of body   This study was approved by the Bioethics Committee
            composition in early adolescence and is associated with   of the Institute of Physiology of the National Academy of
            certain cognitive functions, while also being partially   Sciences of Belarus (protocols No:1 on January 22, 2021,
            influenced by environmental factors.               and No:2 on February 2, 2022) and was conducted in
              Pathological changes in the state of the hippocampus   accordance with the guidelines set forth by the European
            in  obesity  in humans have  been  less  studied,  although   Convention for the Protection of Vertebrate Animals (ETS
            associations have been made between the state of the   No. 123).
            hippocampus and several neuropathological processes.    The rats were euthanized by decapitation under
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            However, there is evidence that a high-calorie diet (HCD)   anesthesia induced  with  sodium  thiopental.  Female  rats
            and physical inactivity, which promote obesity and diabetes,   were euthanized during the diestrus phase of the estrous
            are risk factors for hippocampal neurodegeneration and   cycle, determined by the type of cells present in vaginal
            cognitive impairment.  It has been suggested that diet-  swabs. 12
                              10
            induced obesity may lead to impaired neuronal plasticity   The body weight of the rats was measured using
            in the hippocampus, which in turn may contribute to
            cognitive decline, emotional disturbance, and hyperphagia.   a  weighing  scale  (Saturn  ST-KS7230,  China).  After
            Adipose tissue regulates hippocampal function through   euthanasia, the visceral fat was collected and weighed on a
            the release of adipokines, which may directly or indirectly   laboratory weighing scale (Scout Pro, China). For male rats,
            modulate both neural plasticity and neuroinflammation.    the visceral fat mass included paranephral and epididymal
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            However,  the potential  mechanisms  by which  adipose   fat deposits, while for female rats, it included paranephral
            tissue inflammation in obesity leads to neurodegeneration   and periovarian fat deposits. The mass coefficient (MC) of
            and neuroinflammation in the PFC and hippocampus   the visceral fat was calculated using the following formula:
            remain poorly understood.                          MC = (Visceral fat mass/Body weight) ×100%   (I)


            Volume 4 Issue 1 (2025)                         81                              doi: 10.36922/gtm.5000
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