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CPB 25

The document discusses metabolic processes in the fed and fasting states. In the fed state, insulin levels are high, promoting anabolic processes like glycogen, protein, and triglyceride synthesis in the liver, adipose tissue, and muscle. The brain relies solely on glucose. In the fasting state, insulin levels decrease and catabolic processes like gluconeogenesis and lipolysis are increased to break down substrates for energy and glucose production, especially in the liver. The document also describes how hormones regulate these processes and the pathophysiology of type 2 diabetes, which is characterized by insulin resistance.

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Kristin Douglas
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45 views2 pages

CPB 25

The document discusses metabolic processes in the fed and fasting states. In the fed state, insulin levels are high, promoting anabolic processes like glycogen, protein, and triglyceride synthesis in the liver, adipose tissue, and muscle. The brain relies solely on glucose. In the fasting state, insulin levels decrease and catabolic processes like gluconeogenesis and lipolysis are increased to break down substrates for energy and glucose production, especially in the liver. The document also describes how hormones regulate these processes and the pathophysiology of type 2 diabetes, which is characterized by insulin resistance.

Uploaded by

Kristin Douglas
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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CPB 25: Dietary States and Metabolic Processes Discuss organ inter-relationships in the fed and fasting states

Fed state Plasma glucose, amino acids, triglycerides


Control: Insulin: secretion by the pancreas Response: Anabolic (building of small to larger) o Liver: makes glycogen, proteins and triglycerides (VLDL) Carbohydrate: Glycogen synthesis, glycolysis, hexose-monphos path Gluconeogenesis Fat: Fatty acid and triglyceride synthesis Amino-acid: Amino acid degradation and protein synthesis o Adipose: makes triglycerides Carbohydrate: Glycolysis, hexose-monophosphate path, glucose transport to adipocytes Fat: Fatty acid and triglyceride synthesis o Muscle: Carbohydrate: Glycogen synthesis and glucose transport Fat: FAs are less important than glucose as fuel Amino-acid metabolism: Protein synthesis and uptake of BCAA o Brain Carbohydrates: Brain uses only glucose as fuel ( glucose = problems) Fats: Very little triglycerides in brain (FA cant cross blood-brain barrier) Fasting state Plasma glucose, amino acids, triglycerides Control: Insulin: secretion by the pancreas Response: Catabolic (breaking down of large to small) o Liver Carbohydrate: Gluconeogenesis (creating glucose from pyru. lact, etc.) Glycogenolysis (breakdown of glycogen) Fat: -oxidation of FA and ketogenesis o Adipose: Carbohydrate: Glucose uptake reduced, reducing FA/TG biosynthesis Fat: Triglyceride breakdown and FA release, uptake of FA o Muscle: Carbohydrate: Glucose uptake (low insulin levels) Fat: Week 1-2, FA and KB used as fuel, after 3rd only FAs Amino-acid metabolism: Week 1: rapid proteolysis provides AA for gluconeogenesis; reduces as brain begins to use KB as fuel. o Brain First Days of fasting: Glucose as fuel, blood glucose maintained by hepatic gluconeogenesis from AA precursors of muscle (Cori cycle) 2-3 weeks of fasting: Plasma KB rise, brain begins to metabolize KB as well as glucose. Reduces the need for muscle proteolysis.

Describe hormonal participation in tissue /substrate integration


Insulin: Glycogenolysis, gluconeogenesis, ketogenesis o Activate another protein kinase which causes dephosphorylation Glucagon and Epinephrine: Glycogenolysis, gluconeogenesis, ketogenesis o Activate cAMP-dependant protein kinase A promoting phosphorylation

Describe the nature of Type II Diabetes (pathophysiological example)


Reduced insulin production and end organ resistance Onset in adulthood (obesity usually associated with it ) Accounts for 90% of diagnosed diabetes cases Managed by diet, exercise, oral hypoglycaemic drugs (+/- insulin)

Untreated Type II Diabetes 1. Hyperglycaemia increased hepatic gluconeogenesis, decreased peripheral glucose use **Ketosis is minimal/absent in type II because of low levels of insulin ketogenesis 2. Hypertriglyceridaemia The amount of Fas being released swamps the capacity of oxidation and ketogenesis. Excess FAs converted to TGs which are packaged and secreted as VLDL by the liver.

*Type I no insulin secretion at all (hyperglycaemia, ketosis, hypertriglyceridemia, diabetic ketoacidosis)

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