ENERGY METABOLISM KATRIN ROOSITA, MSI.

METABOLISME ENERGI……

Fig 1. METABOLISM

(Courtesy: Rimbawan, 2007)

Organ utama

pengaturan

metabolisme: hati,

jaringan lemak

(adipose), otot , dan

otak.

Peran: penyimpanan,

penggunaan dan

penyediaan sumber

energi (substrat).

SISTEM PENGATURAN

METABOLISME

SISTEM HORMON

SISTEM SARAF

KETER SEDIAAN

SUBSTRAT

Hubungan

substrat – hormon- sistem

saraf

Substrat (glukosa dan protein)

mempengaruhi sekresi hormon

Hormon dan sistem saraf mengatur

metabolisme dan transport substrat.

HORMON UTAMA METABOLISME

http://www.medbio.info/Horn/PDF%20files/

homeostasis_2a.pdf

1 mmol/L = 18 g/dL

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

Penurunan Kadar glukosa darah & sekresi hormon

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

Fungsi insulin di sel target

en.wikipedia.org

Molecular mechanisms of insulin signaling.

Rask-Madsen C , and Kahn C R Arterioscler Thromb Vasc Biol. 2012;32:2052-2059

Copyright © American Heart Association, Inc. All rights reserved.

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

CONTOH:

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

Aktivitas insulin di Sel Target

Ketersediaan Substrat

Berbeda antara kondisi:

- post absorpsi

- puasa/starvation

- olahraga berat

- terjadi gangguan metabolisme dan kondisi

sakit.

POST ABSORPTIVE STATE

2 - 4 HOURS period after

ingestion of a normal meal :

POST ABSORPTIVE STATE

INCREASES in plasma glucose, amino acids, and

triacylglycerols

baby-growths.com

lipogenesis

MECHANISMS OF HEPATIC- AMINO ACID

METABOLISM (in the absorptive period)

The surplus amino acids ARE NOT STORED, but are either:

a. released into the blood for all tissues to use in

protein synthesis,

b. they are with the resulting carbon skeletons being

degraded by the liver pyruvate, acetyl CoA, or TCA

cycle intermediates, these metabolites can be

oxidized for energy or used in fatty acid synthesis.

METABOLISM OF

ADIPOSE TISSUE

in Post Absorptive State

A. Carbohydrate metabolism

1. Increased glucose transport

2. Increased glycolysis:.

3. Increased activity in the hexose monophosphate (HMP) pathway.

B. Fat Metabolism

1. Increased synthesis of fatty

acids.

2. Increased triacylglycerol

synthesis

3. Decreased triacylglycerol

degradation

METABOLISM OF RESTING MUSCLE

in Postabsorptive State

1. Increased glucose transport

2. Increased glycogen synthesis 3. Increased protein synthesis 4. Increased uptake of branched-chain amino acids.

METABOLISM OF BRAIN IN

POSTABSORPTIVE STATE

http://www.medbio.info/Horn/PDF%20files/homeostasis_2a.pdf

FASTING METABOLISM

Fasting

a. an inability to obtain food,

b. the desire to lose weight rapidly,

c. in clinical situations in which an individual cannot eat because of trauma, surgery, burns, and so forth.

Physiology of Fasting: the absence of food, plasma levels of glucose, amino acids, and triacylglycerols fall, triggering a decline in insulin secretion and an increase in glucagon release.

This sets into motion an exchange of substrates between

liver, adipose tissue, muscle, and brain :

1. the need to maintain adequate plasma levels of glucose

to sustain energy metabolism of the brain and other

glucose-requiring tissues.

2. the need to mobilize fatty acids from adipose tissue, and

the synthesis and release of ketone bodies from the

liver, to supply energy to all other tissues.

INSULIN / GLUCAGON RATIO

availability of circulating substrates

CATABOLIC PERIOD: by degradation of triacylglycerol, glycogen, and protein.

Diseases and Blood Sugar

Regulation

Elevated glucose levels are present in diabetes mellitus, Cushing's syndrome, liver disease, and hyperthyroidism.

Decreased glucose levels are present in Addison's disease, hyperinsulinism, and hypothyroidism.

The most prevalent of these diseases is diabetes mellitus (DM).

Type I DM (insulin-dependent or juvenile-onset) diabetes mellitus, when pancreatic beta cells are destroyed by an erroneous attack by the body's own immune system.

Type II DM, insulin secretion is not reduced; however, there is a reduced sensitivity of target cells to insulin, a phenomenon known as insulin resistance. (Paul I, 2007).

Terima kasih atas

perhatiannya

alternativemagazineonline.co.uk

REFERENCES

http://www.medbio.info/Horn/PDF%20files/homeostasis

_2a.pdf. Insulin_Glucagon Role in Metabolism.pdf

Tom Brody. Nutritional Biochemistry, 2nd edition,

Academic Press, 1999

Pamela C. Champe & Richard A. Harvey

Biochemistry, 2nd edition, J.B. Lippincott Company,

Philadelphia, 1994.

Illingworth. 2007. Biochemistry for Biologists

Fitness Training.

www.bmb.leeds.ac.uk/.../bioc1110/index.htm .

Rimbawan, 2007. Metabolism Slides