The Concentration of Glucose in the Mesenteric Art

The Concentration of Glucose in the Mesenteric Arteries, Hepatic Portal Vein, and Hepatic Vein Before and After Eating.
by Nadia Hoxworth

Introduction

When food is taken into the body, it must be broken down into simpler molecules to be absorbed into the blood and lymph (Jones. 2013). Hepatic portal circulation is part of systemic venous circulation: blood from the digestive organs and spleen circulates through the liver before returning to the heart (Jones.2013). During the process of digestion, the capillaries in the liver (through Hepatic Portal circulation) remove glucose from the intestine for its conversion to glycogen (Zaykoski. 2010). Glucose is a carbohydrate, and more specifically, a monosaccharide (a simple type of sugar) (Cummings. 2014). Diets that contain large amounts of carbohydrates elevate blood glucose levels (Englyst, Hudson, Cummings. 1999). Glucose is denoted as C6H12O6. It is found in fruits, plants, the human body, some forms of bacteria, and some fungi (Cummings. 2014). Glucose is the source of energy for all of our body functions, especially the brain. The only energy the brain can use is from glucose. Glucose is also the primary source of energy for muscles, backed up by other sources if it runs out (Bemstein. 2012). About 75% of glucose consumed during a meal is stored as glycogen in the liver. As humans do not feed continuously (fasting), the production of glycogen from a meal ensure that supply of glucose will be available for several hours after meal. When glucose levels in the plasma fall below a certain value, the alpha cells of the pancreas are stimulated to release the hormone glucagon. Glucagon stimulates the breakdown of stored glycogen (in the liver) into glucose, which is then released back into the blood (trough hepatic veins). When glucose levels in the plasma increase, the beta cells of the pancreas are stimulated to release the hormone insulin. Insulin is vital to the regulation of plasma glucose levels, or “blood sugar,” because the hormone enables cells to absorb glucose from the bloodstream (Zao, Stabler, Smith, Locuta, Griff. 2014).
a) Experiment examine concentration of glucose in the Mesenteric Arteries, Hepatic Portal Vein, and Hepatic Vein before and after meals.
b) The greatest glucose level after meal will be in the Hepatic Portal Vein. The greatest glucose level before meal will be in the Hepatic Vein.

Materials and Methods.

Metric ruler, 6 test tubes, clock, test tube rack, marking pen, beaker, hot plate, Benedict’s reagent, postprandial samples (after eating): mesenteric artery (A1), hepatic portal vein (B1), hepatic vein (C1), fasting serum samples: mesenteric artery (A2), hepatic portal vein (B2), hepatic vein (C2).
This test was qualitative. Six tubes were marked with a metric ruler at 1 cm to represent the volume of serum and 2 cm to represent the volume of reagent. Those tubes was labeled according to the blood vessel from which the sample of serum were taken: postprandial samples (after eating) are mesenteric artery (A1), hepatic portal vein (B1), hepatic vein (C1); fasting serum samples are mesenteric artery (A2), hepatic portal vein (B2), hepatic vein (C2). Postprandial and fasting tubes were filled with 1 cm. of serum. When on a hot plate with a big beaker boiling water was prepared, postprandial (after eating) tubes were filled with 2 cm. of Benedict‘s reagent (blue) and heat in the water bath for 3 minutes. Color change and time were recorded.
The same amount of reagent was added to fasting tubes and heat in the water bath for 3 minutes. Color change and time were recorded.

Results.

When postprandial samples A1, B1, C1 (Table 1) were filled with Benedict’s reagent and heat in the water bath, the first color change happened at 42 seconds in B1 tube, which color turned from blue to orange. The other color change happened in C1 tube at 1 min, which color turned from blue to orange. The A1 tube from blue turned to translucence red at 2 min. After 3 minute the final colors for postprandial samples are: A1- translucent red/ B1- red/ C1- dark red.
When fasting serum samples A2, B2, C2 (Table 2) were filled with Benedict’s reagent and heat in the water bath, the first color change happened at 46 seconds in C2 tube, which color changed from blue to orange. The other color change happened in 1 minute 35 seconds in A2 tube, which color changed from blue to brownish blue. The B2 tube at 2 minute 15 seconds did not change color. After 3 minute the final colors for fasting serum samples are: A2- blue on a bottom, brownish-reddish on top/ B2- blue on a bottom, dark orange on top/ C2- red.

Table 1: Postprandial glucose concentration in blood vessels.
Serum
Order of color change
           Final color
Mesenteric Arteries (A1)
2 min/ light orange
translucent red
Hepatic Portal Vein (B1)
42 sec./orange
red
Hepatic Vein (C1)
1 min.-/orange
dark red

Table 2: Glucose concentration in blood vessels during fasting.
Serum
Order of color change
                Final color
Mesenteric Arteries (A2)
35 sec./ brownish-blue         
blue on a bottom, brownish- reddish on top
Hepatic Portal Vein (B2)
2min. 15 sec. / no color change
blue on a bottom, dark orange on top
Hepatic Vein (C2)
46 sec. / orange
red

Discussion.

Experiment examines concentration of glucose before and after meals in the Mesenteric Arteries, Hepatic Portal Vein, and Hepatic Vein. Hypothesis state that
greatest glucose level after meal will be in the hepatic portal vein, and the greatest glucose level before meal will be in the hepatic vein. According to the data analysis  (Table1, Table2) the hypothesis is supported. Data analysis shows that Benedict’s reagent as an indicator of glucose changed color from blue to red. Blue color indicates a negative glucose levels, and red color indicates positive glucose levels. Other colors like orange, brownish-reddish or dark orange indicate some presence of glucose.
Postprandial Table 1 shows that most presence of glucose is in Hepatic Portal Vein. After meal intake, liver, pancreas, and intestinal enzymes help to break the food down for easier absorption in the large intestine (Zaykoski. 2010).  This process lead to increase blood glucose levels. When glucose levels rise, it leads to the production of insulin, which decrease glucose levels, keeping glucose levels in the blood in a normal range. A normal fasting blood glucose target range for an individual without diabetes is 70-100 mg/dL (3.9-5.6 mmol/L). The American Diabetes Association recommends a fasting plasma glucose level of 70–130 mg/dL (3.9-7.2 mmol/L) and after meals less than 180 mg/dL (10 mmol/L) (Davidson, Moreland. 2013).  From intestine glucose travels through Hepatic Portal Vein to the liver where it will be store for future use when glucose levels will decrease. Data analysis (Table 1) confirms this result.
Fasting data analysis (Table 2) shows that the highest glucose concentration is in Hepatic Vein. The liver stores excess glucose as glycogen. During the fasting blood glucose levels drop down, and pancreas release hormone glucagon, which is raises the blood glucose level by increases the liver’s conversion of glycogen to glucose (Jones. 2013). That is why fasting data table shows great amount of glucose in Hepatic Vein where glucose travels from the liver to Inferior Vena Cava to pulmonary and systemic circulation.
When pancreas does not produce enough insulin, glucose remains in the bloodstream, and the body’s cells are unable to take it up to serve as the primary fuel for metabolism (Zao, Stabler, Smith, Locuta, Griff. 2014). If fasting samples and postprandial would be from the person who has Diabetes Mellitus Type 1, results of experiment would be different. The Mesenteric Arteries after food intake would probably have high amount of sugar concentration because pancreas would not be able to release insulin. After fasting, glucagon will increase glucose levels by stimulate liver to release glucose from glycogen.
During the experiment were a few sources of errors. The most challenging part of designing an experiment is trying to control time and color change in 3 beakers, which might affect the result. Source of error might be contaminated test tubes. Possibly excess or not enough heat in the water baths could alter results.

Clinical Applications.

Keeping glucose levels concentration in blood at the normal range is absolutely necessary. Diabetes mellitus is one of the most common and chronic diseases all over the world. It is characterized with either insulin deficiency or insulin resistance (Tarihi.2012). Precise glucose control has been shown to reduce and delay the onset of the serious chronic complications of diabetes (Martini, Welch. 2012) Complications of diabetes include accelerated coronary artery disease, kidney failure. Degenerative changes in cardiac circulation can lead to accelerated coronary artery disease and early heart attacks. Other peripheral changes in the vascular system can disrupt normal circulation to the limbs. For example, a reduction in blood flow to the feet can lead to tissue death, ulceration, infection, and loss of toes or major portion of one or bother feet (Martini, Welch. 2012).
Type 1 diabetes is insulin dependent. When insulin concentrations decline, cells can no longer absorb glucose; tissues remain glucose starved, despite the presence of adequate or even excessive amounts of glucose in bloodstream. After a meal rich in glucose, blood glucose concentrations may become so elevated that the kidney cells cannot reclaim all the glucose molecules that enter the urine. The high urinary concentration of glucose limits the ability of the kidneys to conserve water, so the individual urinates frequently and may become dehydrated. Despite high blood concentrations, glucose cannot enter endocrine tissues, and the endocrine system responds as if glucose were in short supply. Pancreatic alpha cells release glucagon, and glucocorticoid production accelerates. Peripheral tissues then break down lipids and proteins to obtain the energy needed to continue functioning. The breakdown of large numbers of fatty acids promotes the generation of molecules called ketone bodies. These small molecules are metabolic acids whose accumulation in large numbers can cause a dangerous reduction in blood pH (Martini, Welch. 2012).
A diagnosis of diabetes mellitus is based on two observations: a high fasting blood glucose and the persistence of an elevated blood glucose level two hours after drinking a fixed amount of glucose. Careful control to avoid high glucose levels and keep the long-term marker (hemoglobin A1C) at a low level has been shown to reduce the risk of chronic kidney, eye, and cardiovascular complications (Martini, Welch. 2012)

Work Cited

Bemstein, G. Why We Need Glucose (A Biological History). Helthline. Web. 31 Jan. 2012. <http://www.helthline.com/health-blogs.>
Cummings, T. The History of Glucose. Web. 2014.  Davidson N., Peggy Moreland. Know Your Blood Glucose Target Range. Mayoclinic. Web. 8May. 2013. http://www.mayoclinic.org/disease-conditions/diabetes/
Englyst, Hudson, Cole, John Cummings. Rapidly Available Glucose In Foods: An In Vitro measurement That Reflects The Glycemic Response. American Society for Clinical Nutrition. 1999.
Jones, S. Pocket Anatomy And Physiology, 2th edition. F. A. Davis Company. 269, 207pp.
Martini, F., Kathleen Welch. A & P Applications Manual. Frederic H. Martini. 113,114pp.
Tarihi, K. Insulin Hormone: Mechanism and Effect on the Body and Relationship with Central Nervous System. Dicle Medical Journal. 2012.
Zaykoski, L. The Importanse of Hepatic Circulation in Human Body. Brighthub. Web. 28 Feb. 2010. http://www.brighthub.com/science/medical/articles/65425.
Zao, P., Stabler, T., Smith, L., Locuta, A., Edwin Griff. PhysioEx 9.1 Laboratory Stimulations in Physiology. CD-ROM. Person Education. 2014.


Рецензии