Introduction
The rise of obesity has increased dramatically due to our lifestyle, how our food is prepared and our consumption of convenient fast food at our finger tips. In the case study that I will be discussing it’s about a 18year old male, known as John, and for his age he is overweight by 40 kilograms. His level of obesity, is due to his consumption of a very high rich carbohydrate diet, especially in the form of ‘junk food’. If John continues on this journey, he is at a very high risk of becoming a type II diabetic, high risk of cardiovascular disease and other related metabolic disorders.
Carbohydrate Metabolism
To understand the end to end process of how carbohydrates are utilised in the body, we firstly have to define metabolism. Metabolism is all biochemical reactions that take place in a living organism. It can be broken up into two major categories catabolism and anabolism. The processes related to degradation of complex substances such as polysaccharides, lipids, proteins known as catabolism. The synthesis of complex organic substance such as proteins from amino acids is called anabolism. Both catabolism and anabolism occur in three different stages of complexity, but to put it simply the stages are, digestion, absorption and metabolism of what we consume to feed our bodies to create energy and to function.
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The process of digestion, begins in the mouth. Saliva in the mouth contains starch-digesting enzymes (known as salivary amylase), helps breakdown the complex carbohydrates by hydrolysis of the glycosidic linkages. The polysaccharides are pass through the stomach and into the small intestine, where pancreatic amylase which will further hydrolysis the polysaccharides to disaccharides, such as maltose, sucrose and lactose. These disaccharides are hydrolysis by enzymes which are located in the intestinal mucosal cells. The enzymes known as maltase, sucrase and lactase play an important role in converting disaccharides into monosaccharides (glucose, fructose and galactose), which are able to be transport via active transport mechanism into the blood stream. Active transport is the way the body absorbs glucose, fructose and galactose across the cell membrane, which requires energy, such as Adenosine Triphosphate (ATP) and protein transport carriers which allows the monosaccharides to move across the cell via sodium-potassium pumps. The energy is only expended to keep the sodium gradient active and not for the transport for the monosaccharides itself. Once monosaccharides have crossed intestinal wall via active transport mechanism, into the blood stream its transported to the liver. Insulin will promote the movement of monosaccharides into the cell to start the process of glycolysis.
Glycolysis is the central metabolic pathway which plays a central role in every living organism to generate energy and metabolic intermediates. Glycolysis is a 10-step process, by using different enzymes catalysts to assist with that conversion of one molecule of glucose to two molecules pyruvate, generation of two molecules of energy in the form of ATP and NADH coenzymes. Glycolysis can be split up into two stages; energy consuming phase and energy generating phase. Energy consuming phase consists of steps 1 to 3 of glycolysis where Glucose is converted to Fructose 1,6-bisphophate and were two ATP are expended in the process. Energy generating phase is the last 6 steps in glycolysis is where Fructose 1, 6-bisphosphate becomes the end products of two pyruvate, two NADH and two ATP. Pyruvate is oxidised to Acetyl CoA, under oxygen rich conditions, and is the entry point for aerobic respiration which consists of three very important processes; Citric Acid Cycle (CAC), electron transport chain and oxidative phosphorylation. The oxidative reactions in CAC generate reduced electron carriers which drive ATP production.
Even though aerobic respiration is a vital part of carbohydrate metabolism, there is a process that comes into the effect when there is high rich carbohydrate diet is involved and that process is lipogenesis. Lipogenesis is the metabolic pathway by which fatty acids are synthesized from Acetyl CoA. As we know acetyl-CoA the end product of oxidation of pyruvate. As Acetyl-CoA is generated in the mitochondria and lipogenesis is in cytosol. Acetyl-CoA is transport to the cytosol to be converted to malonyl-CoA by the enzyme acetyl CoA – carboxylases 1 (ACC1). The malonyl-CoA is converted to palmitate, which is first fatty acid product of lipogenesis. Palmitate under goes further degradation to generate complex fatty acids. This whole process of lipogenesis is only activated once there is dietary intake has increased.
Obesity and Type II Diabetes
As mention in the introduction, our case study is focused on a high rich carbohydrate diet, a young man who is obese and on the verge of type II diabetes. From scientific prospective obesity is the increase size of adipose tissue that store fats. Medical cause of obesity is not just from eating large amounts of foods, rich in carbohydrates and lipids, but it can be linked to genetic or endocrine disorders as well. Obesity is also a precursor to other medical concerns, such as type II diabetes, insulin resistance disorders, cardiovascular disease, and cancer just to name a few.
In part 1, lipogenesis is part of lipid metabolism, is activated when there is over cumulation of nutrients needed for energy requirements. These energy requirements can come from consumption of fats, carbohydrates or proteins. In this case the increase carbohydrates stimulate lipogenesis in the both the liver and adipose tissue and storage of fatty acids which is the end product of lipogenesis. With this increase in storage of fatty acids in the adipose tissues become overloaded and the excess fatty acids are stored outside the adipose tissues, which causes the increase in weight gain in an individual.
The case study about John, the overweight 18-year-old being at risk of developing type II diabetes. One of the precursors to type II diabetes in overweight/obese individuals, like John, is the development of insulin resistance. Insulin resistance is where the body at a cellular level response becomes sensitive and resist the signalling of insulin and with this sensitivity the pancreas becomes overworked to keep the blood glucose levels at the correct levels. Insulin resistance increases there is a probability that the individual will develop type II diabetes.
Type II diabetes is when your pancreas is unable to make the right amount of insulin it needs to work effectively. As we mention in part 1, insulin is important to assist the transportation of glucose into the cell from the bloodstream, to start the beginning of glycolysis to produce energy for the body to function. The common symptoms of type II diabetes are fatigue extreme thirst, frequent urination, extreme hunger, weight loss, infections, healing of wounds is slow, and blurry vision.
References
- Stoker, S. (2018). General, Organic & Biological Chemistry (7th ed.). Boston, MA: Cengage Learning.
- Mathews, C. & van Holde, K. (1996). Biobchemistry (2nd ed,). Menlo Park,CA: The Benjamin/Cummings Publishing Company.
- Barasi, M. E (2007). Nutrition at a glance. Oxford, UK: Blackwell Publishing.
- Boron, W. F., & Boulpaep, E. L. (2005). Medical physiology. Oxford: Elsevier.
- Smith, U., & Kahn, B. B. (2016). Adipose tissue regulates insulin sensitivity: role of adipogenesis,de novo lipogenesis and novel lipids. Journal of Internal Medicine, 280(5), 465–475. doi: 10.1111/joim.12540
- BIOB111_Assignment 1_Melanie Vasen 2 | Page
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