SAQUITON, Ma. Frances B.

Section 9

A Case Study on Carbohydrate Metabolism

1. Based on the article, what causes skin aging?

Human skin aging is caused by two processes namely intrinsic and extrinsic aging.

First, intrinsic aging is inevitable because it naturally occurs and is usually rooted in the things

that happen inside the body. It can be caused by hormone level imbalances and sudden changes

in our cells and protein makeup. As an individual ages, hormones such as estrogen and

progesterone linked with menopause, and androgens affect the skin as the body works with

these hormones to maintain equilibrium. Skin issues such as dryness, wrinkling, and loss of

elasticity will develop once this balance is disturbed. Second, extrinsic skin aging is the

consequence of external factors and lifestyle choices an individual makes. It is commonly a

result of unprotected exposure to ultraviolet (UV) radiation which then causes

hyperpigmentation and skin discoloration. Having a poor diet also contributes since free radicals

and the glycation process are more likely to occur affecting collagen production. Also, intrinsic

skin aging can be worsened by extrinsic skin aging but it is more preventable. Loss of skin

moisture is also related to skin aging (Papakonstantinou, 2012).

2. What is the structure of HA made up of?

The extracellular matrix (ECM) functions as a structure and support for the

human body and it is comprised of elastin and collagen. Both are fibrous elements that are

surrounded by Hyaluronic acid or hyaluronate wherein it is a molecule that serves in

maintaining the moisture of an individual’s skin. HA has an uncomplicated composition but it

also has distinct properties such as not being attached to a core protein, unlike other

glycosaminoglycans (GAG). At the same time, it has the ability to group with heavily

glycosylated proteoglycans as a non-sulphated glycosaminoglycan. HA has steady tertiary

structures in aqueous solutions and it is high in resistance wherein solutions flow slower due to

friction than a fluid with low viscosity. In line with this, HA is considered a vital piece of the

extracellular matrix as it aids during matrix restructure. It is also essential in the tissue

regeneration process or tissue repair, and cell signaling (Papakonstantinou, 2012).      

3. HA is most abundant in what human body part?

According to the study conducted by Papakonstantinou (2012), the skin

comprises fifty percent Hyaluronic acid (HA) in humans and considered to have the greatest

concentrations of HA. Alongside it, the fluid inside the eye or the vitreous humor comprises a

large amount of HA that functions as a carrier of nutrients and shock absorbers for the eye, the

HA in the umbilical cord sustain its elasticity, and the HA in a synovial fluid acts like a viscous

fluid for its purpose as a lubricant solution. Hyaluronic acid is also found in the tissues and fluids

of the human body. It is capable of forming gelatinous fluid thus, acts as a cushion.
4. List the functions of HA in the body.

Based on a study conducted by Papakonstantinou (2012), first, hyaluronic acid

supplies a framework in between an individual’s skin layers which aid in its overall cellular

functions such as ion exchange and transport of compounds. Second, HA hydrates and

nourishes collagen as it binds with water thus, keeping the skin free from wrinkles, drying, and,

aging. It maintains water equilibrium inside the body and retains the skin’s moisture and

elasticity. Third, HA is determined to be a lubricant for joint tissues because of its jelly-like

characteristic. It also aids in promoting the growth and development of cells and tissues. Fourth,

HA is important in the tissue regeneration process or wound healing wherein an HA that has a

high molecular weight initiates immunosuppressive and anti-inflammatory properties. Fifth, a

decrease in the size of an HA acts as a signal of inflammation that is occurring inside the body.

Lastly, the levels of HA found in cancer cells correspond with the possible aggression of the

tumor an individual has. 

5. What enzymes are involved in the synthesis of HA?

Hyaluronic acid synthase (HAS) is the membrane-bound enzyme involved in the

synthesis of HA polymer. It is considered homologous in structure and is grouped as a

glycosyltransferase. It is encoded into three classes of enzymes namely HAS1, HAS2, and HAS3

that have distinct functional characteristics and enzymatic activity. HAS varies in both product

size and kinetic properties wherein the existence of the three classes of enzymes indicates that

the roles performed by HA are being controlled. It is regulated at the activities undertaken by

HAS isoforms (Papakonstantinou, 2012).

6. What happens during HA degradation?

During hyaluronic acid degradation, HA is degraded into hyaluronidases

(HYAL) wherein six categories have been developed including HYAL-1, HYAL-2, HYAL-3, HYAL-4,

PH-20, and HYALPI. Present studies have found that HYAL-1 is in serum and mutations were

related to HYAL deficiency, HYAL-2 hydrolyzes HA that has a high molecular weight, and HYAL-3

may be useful in HA degradation with the assistance of HYAL-1. In line with this, HYAL-3 is

fragmented in human lungs, bone marrow, and testis (Papakonstantinou, 2012).

7. How is HA degraded non-enzymatically?

A free-radical mechanism necessitates molecular oxygen and it usually occurs

when there is an occurrence of the generation of a reactive free radical that will respond with

stable molecules in order to create new free radicals. This process is where hyaluronic acid is

degraded non-enzymatically. Reducing agents including thiols, cuprous ions, ferrous, or ascorbic

acid comprise it. Consequently, a delay caused by these agents in the free-radical mechanism

may become a benefit for the skin because of its moisturizing properties (Papakonstantinou,

2012).

8. What is the significance of having high levels of HA in the dermis?

Elevated levels of hyaluronic acid are integrated during scar-free tissue repair.

The presence of HA in the dermis constitutes water homeostasis, osmotic pressure, and

electrostatic interactions that will stabilize the various structures of the skin. Also, dermal HA
stands as a major component to strengthen skin hydration in order to act against skin aging

brought by intrinsic and extrinsic aging (Papakonstantinou, 2012).

9. What causes premature skin aging?

Based on a study conducted by Papakonstantinou (2012), prolonged exposure to

UV radiation often leads to premature skin aging also referred to as photoaging. Its damaging

effect alters the normal skin structures of an individual mainly the ECM of the connective tissue.

Thus, speeding its natural aging process as the skin collagen is reduced. UV exposure also

amplifies the deposition of HA and the release of histamine from mast cells. It then triggers an

inflammatory response on the skin wherein an accumulation of scar-like type I collagen will be

observed, a rather different type of skin healing.

10. Note what observations were made about intrinsic skin aging? What is the result of this

inevitable physiological process?

According to the study conducted by Papakonstantinou (2012), findings of the

tissue specimen of photoprotected skin in both male and female indicate that intrinsic skin

aging may be caused by a lowered HA levels and reduced HAS-1, HAS-2, a glycoprotein called

CD44 antigen, and receptor for Hyaluronan-mediated motility or RHAMM. Hence, resulting in

skin dryness accompanied by the aging of human organs and tissues. This inevitable

physiological process ends with a conclusion that indeed, intrinsic skin aging has a wide

distinction from extrinsic skin aging. Future studies shall be conducted again as the information

that will be gathered will help in various discoveries. It includes regulation of an individual’s skin
moisture, improvement of contemporary drugs, and medicines, and possible treatments for the

aging of the skin.

References:

Papakonstantinou, E., Roth, M., & Karakiulakis, G. (2012). Hyaluronic acid: A key molecule in skin

aging. Dermato-endocrinology, 4(3), 253–258. https://doi.org/10.4161/derm.21923