Eight weeks consumption of high-fat diet promotes Mesenteric fat deposition when compared to other rat diets

Khairil Azwan¹, Resni Mona¹, Jannathul Firdous¹, Dina Keumala Sari³, Pamela Rosie David², Noorzaid Muhamad¹*

¹Cluster for Integrative Physiology and Molecular Medicine (CIPMM), Faculty of Medicine,

Royal College of Medicine Perak, Universiti Kuala Lumpur, Jalan Greentown, 30450 Ipoh, Perak, Malaysia.

²Department of Anatomy, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia.

³Nutrition Department, Faculty of Medicine, Universitas Sumatera Utara, Indonesia.

*Corresponding Author E-mail: noorzaid@unikl.edu.my

ABSTRACT:

Metabolic syndrome is a grouping of several medical conditions plaguing the modern world today. Excessive visceral fat is strongly associated with abdominal obesity which is one of the characteristics of metabolic syndrome. In general, an unbalanced, rich diet plays an important role in the proliferation of adipocytes. Our aim is to observe which diet contributes to the deposition of visceral fat such as the mesenteric fat. For eight weeks, thirty-five Sprague Dawley rats were divided into five groups and were fed five different types of diets. The five diets are normal rat chow, high sugar, high starch, high protein and high fat rat (palm oil-based) feed formula. Besides the formularized rat feeds, the rats were given tap water ad libitum. The result showed high fat diet promotes mesenteric fat proliferation when compared to other rat feed formula. Present study showed that high-fat diet promotes mesenteric fat proliferation when compared to other diets.

KEYWORDS: Diet, Enzymes, High-fat, Mesenteric fat, Palm oil.

INTRODUCTION:

Obesity is tightly associated with lifestyle mismanagements and most likely to result in diabetes mellitus, hyperlipidemia, and hypertension¹. Abdominal obesity or more specifically visceral obesity is a condition used to characterize metabolic syndrome. Excessive visceral fat also is associated with cardiovascular disease, vascular diseases and show a strong association with type 2 diabetes. Visceral fat found in the mesentery, which is a fold of peritoneum attaching the small intestine to the posterior abdominal wall, is called mesenteric fat. Treatment of obesity has been a focus worldwide and this includes searching for its origin and solving it with modern medicine or even medicinal plants².

Despite the many factors contributing to obesity, much research suggests that environmental, especially dietary factors are a major contributor to the obesity epidemic which also is a co-factor for metabolic syndrome³. Lipids for example, are widely involved in oxidative reactions and oxidative stress in cells is associated with grave illnesses such as cancer, atherosclerosis, heart disease, general inflammation and even anaemia⁴. The deleterious effects of oxidation stress have propelled extensive research on the cure such as antioxidants, pharmaceuticals etc⁵. Developed countries in the west included fiscal measures such as taxation on unhealthy (fat and sugars) and subsidies on healthy (fruits and vegetables) food to tackle the effects of calorie-dense foods⁶.

To evaluate preventive measures and the underlying pathologies of metabolic syndrome, many experimental animal models using different kinds of diets have been researched⁷. Several weeks of consumption of diet with fat content of more than 40% leads to obesity, hypertriglyceridemia and hyperglycaemia in rodents, painting a very similar picture to human obesity and metabolic syndrome characteristics⁸. Hyperlipidemia is indicated to be a major health issue and its complications include atherosclerosis, stroke and heart attack⁹.

MATERIALS AND METHODS:

Thirty-five male Sprague Dawley rats aged 8 weeks old were kept in a constant temperature room (22 degree Celsius) with alternating daylight and night cycle. The rats were divided into five groups (n=7) after two weeks of acclimatization. Each group were fed a specified rat feed formula each day for eight weeks ad libitum and supplied with tap water as drinking water.

The rat feed formulas’ macronutrients are as follows: Control (standard rat chow macronutrients), high-fat (35% fat), high-protein (52% protein), high-sugar (96% glucose) and high-starch (83% carbohydrates).

After eight weeks, the rats were euthanized using carbon dioxide. The abdomen of the rats was dissected, and the mesentery was spread out as shown in the pictures. The gross appearances of the mesentery were observed, pictures taken and compared between the groups.

All animal ethics practices are in compliance with the guidelines approved by the FOM IACUC University of Malaya (Ref: 2019-21114/UNIKL/R/KAMJ)

RESULTS AND DISCUSSION:

Fats and oils are important constituents of foods and is considered as one of the prime areas in food processing industry of a country¹⁰. Palm oil is one of Malaysia’s main produce and export and it is used widely locally and regionally. This makes palm oil the source of fat of choice for our high-fat feed. Instead of using lard, olive oil or other kinds of oil, palm oil is more familiar to everyday local food and is a staple for years.

Many research and studies have proven that a diet high in fat content will be detriment to a person’s health. One similar study induced chronic hyperlipidemia in wistar rats after being fed coconut oil and ghee for eight weeks¹¹. Two research showed that feeding rats food with 16% butter formula for only four weeks could result in hyperlipidemia and clinical obesity^12,13. An experiment using rat feed with 45% of energy from lipids plus 17% of energy from sucrose showed to promote obesity and an increase in adipose tissue size and number¹⁴. Several experiments report high fat (10% sucrose, 35% starch, 25% soybean oil) diet feeding to rats for 3 months produces glucose intolerance with normal fasting glucose level^15,16. A 'western' high fat diet (21.4% fat) combined with a high fructose drink was noted to be the mutable cause of metabolic syndrome development with hepatic and vascular pathology¹⁷.

A quality protein intake was shown to have an inverse relationship with visceral fat deposition¹⁸. This information agrees with our observation of the gross mesenteric fat of the high-protein group which showed less mesenteric fat deposition as shown in Figure 2. It was also observed that the high-fat group has the most mesenteric fat deposited compared to the other groups. Mesenteric blood vessels are visible in other groups except the high-fat group as the well deposited fat obscures the blood vessels. A study revealed that a high-fat diet increased visceral adipocyte hypertrophy histologically, increased adipose tissue inflammation and accompanied by elevated biochemical markers with signalling pathways of lipid accumulation¹⁹.

A high-fat diet consumption increases the chance to develop obesity and it is characterized by large visceral adipocytes and increased visceral adipose inflammation²⁰. One research confirmed the effects of high-fat diet on adipose tissue, in which increased calories lead the way to increased adipocyte size and stimulated adipocyte precursor proliferation, thereby increasing adipocyte number especially in the visceral fat tissue²¹. Cinti et al. reported that adipocytes in different areas grows differently. Mesenteric adipocytes primarily grow by hypertrophy while retroperitoneal fat grows through hyperplasia when the person becomes obese²².

Albeit rich in vitamin E, palm oil is a diet high in calories and these extra calories are converted into adipocytes in the body²³. Visceral adipocytes contain high 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme activity, and this particular enzyme enhances pre-adipocytes to differentiate into visceral fat proliferation which results in visceral obesity²⁴.

CONCLUSION:

Eight weeks consumption of a palm oil-based, high-fat diet promotes mesenteric fat proliferation when compared to other diets.

ACKNOWLEDGEMENTS:

The authors would like to thank the Malaysian Ministry of Higher Education and Ministry of Science and Technology (MOSTI) for funding this study under the grant FRGS/1/2018/SKK08/UNIKL/03/1.

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Received on 01.03.2021 Modified on 27.06.2021

Research J. Pharm.and Tech 2022; 15(2):571-574.

DOI: 10.52711/0974-360X.2022.00093