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Homeostatic Control of Metabolism

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Presentation on theme: "Homeostatic Control of Metabolism"— Presentation transcript:

1 Homeostatic Control of Metabolism

2 Food Intake How does your body know when to eat?
How does your body know how much to eat? Two ‘competing’ behavioral states: Appetite = desire for food Satiety = sense of fullness

3 Hypothalamic Centers Feeding center – tonically active
Satiety center – inhibits feeding center Figure 11-3

4 Regulation: Classic Theories
Glucostatic theory: glucose levels control the feeding and satiety centers in hypothalamus Low [glucose] – satiety center suppressed High [glucose] – satiety center inhibits feeding center Lipostatic theory: body fat stores regulate the feeding and satiety centers Low fat levels  increased eating Recent discovery of leptin and neuropeptide Y provides support

5 Peptides Regulate Feeding
Input to hypothalamus: Neural from cerebral cortex Neural from limbic system Peptide hormones from GI tract Adipocytokines from adipose tissue

6 Peptides Regulate Feeding
Note the diversity of peptide origins! cholecystokinin =

7 Peptides Regulate Feeding
inhibition Figure 22-1

8 We Eat To Do Work Energy input = energy output
Energy output = work + heat 3 categories of work: Transport work – moving molecules from one side of membrane to the other Mechanical work – movement Chemical work – synthesis and storage of molecules Short-term energy storage – ATP Long-term energy storage – glycogen, fat

9 Metabolism = sum of all chemical reactions in the body
Anabolic pathways – synthesize large molecules from smaller Catabolic pathways – break large molecules into smaller

10 Metabolism Divided into two states: Fed (or Absorptive) state
After a meal Anabolic – energy is stored Fasted (or Post-absorptive) state Molecules from meal no longer in bloodstream Catabolic – storage molecules broken down

11 Fate of Ingested Molecules
Immediate use in energy production: nutrient pools Synthesis into needed molecules (growth, maintenance) Storage for later use Fate depends on type of molecule: carbohydrate, protein, or fat

12 Excess converted in liver Metabolism in most tissues
DIET Fats Carbohydrates Proteins Build proteins Free fatty acids + glycerol Excess stored Protein synthesis Glycogenesis Excess stored Amino acids Glucose Fat stores Lipogenesis Excess glucose Lipogenesis Glycogen stores Body protein Lipolysis Urine Glycogenolysis Glucose pool Gluconeogenesis Free fatty acid pool Range of normal plasma glucose Amino acid pool Many immediately used Excess converted in liver Many immediately used Metabolism in most tissues Brain metabolism Excess nutrients Figure 22-2

13 What Controls This? Hormones control metabolism by altering enzyme activity and molecule movement Push-pull control: different enzymes catalyze forward and reverse reactions

14 Push-Pull Control INSULIN enzyme 1 enhanced, enzyme 2 inhibited
enzyme 1 inhibited, enzyme 2 enhanced GLUCAGON Figure 22-4

15 Metabolism is Controlled by Ratio of Insulin and Glucagon
Anabolic Catabolic Figure 22-9

16 Fed State Many immediately used

17 Fasted State Figure 22-7 1 Liver glycogen becomes glucose. 2
Adipose lipids become free fatty acids and glycerol that enter blood. Triglyceride stores Liver glycogen stores Free fatty acids Free fatty acids Glycerol Glycogenolysis -oxidation Gluconeogenesis Energy production Ketone bodies Energy production Glucose Glycogen Proteins Gluconeogenesis Pyruvate or Lactate Amino acids Ketone bodies Glucose Energy production 3 Muscle glycogen can be used for energy. Muscles also use fatty acids and break down their proteins to amino acids that enter the blood. 4 Brain can use only glucose and ketones for energy. Figure 22-7

18 Pancreas – Islets of Langerhans
Figure 22-8

19 Insulin Origin in β cells of pancreas Peptide hormone
Transported dissolved in plasma Half-life ~5 min Target tissues: liver, muscle, adipose tissue

20 Insulin Secretion promoted by: Secretion inhibited by:
High plasma [glucose] (> 100 mg/dL) Increased plasma amino acids Feedforward effects of GI hormones Glucagon-like peptide-1 (GLP-1) Gastric inhibitory peptide (GIP) Anticipatory release of insulin Parasympathetic input to β cells Secretion inhibited by: Sympathetic input Reduced plasma [glucose]

21 Insulin Mechanism of Action
Extracellular fluid 1 Insulin Insulin binds to tyrosine kinase receptor. 1 2 Receptor phosphorylates insulin-receptor substrates (IRS). 3 Second messenger pathways alter protein synthesis and existing proteins. GLUT4 2 IRS IRS P Transport activity 4 3 4 Membrane transport is modified. Second messenger pathways Nucleus Enzymes or 5 Cell metabolism is changed. 5 Transcription factors Changes in metabolism Figure 22-11

22 Insulin Lowers Plasma Glucose
Increases glucose transport into most insulin-sensitive cells Enhances cellular utilization and storage of glucose Enhances utilization of amino acids Promotes fat synthesis

23 Insulin Increases Glucose Transport
Required for resting skeletal muscle and adipose tissue Moves GLUT-4 transporters to cell membrane Exercising skeletal muscle does not require insulin for glucose uptake In liver cells, indirect influence on glucose transport

24 Insulin Increases Glucose Transport: Skeletal Muscle & Adipose Tissue
GLUT-4 transporters moved to cell membrane Figure 22-12

25 Insulin Increases Glucose Transport: Indirect in Liver Cells
Insulin activates hexokinase, keeps IC [glucose] low Figure 22-13

26 Insulin Enhances Utilization and Storage of Glucose
Activates enzymes for: Glycolysis – glucose utilization Glycogenesis – glycogen synthesis Lipogenesis – fat synthesis Inhibits enzymes for: Glycogenolysis – glycogen breakdown Gluconeogenesis – glucose synthesis

27 Insulin Enhances Utilization of Amino Acids
Activates enzymes for protein synthesis in liver and muscle Inhibits enzymes that promote protein breakdown (no gluconeogenesis) Excess amino acids converted into fatty acids

28 Insulin Promotes Fat Synthesis
Inhibits β-oxidation of fatty acids Promotes conversion of excess glucose into triglycerides Excess triglycerides stored in adipose tissue

29 Energy storage Glucose metabolism Figure 22-14

30 Glucagon Origin in α cells of pancreas Peptide hormone
Transported dissolved in plasma Half-life ~5 min Target tissues: mostly liver α cells require insulin to uptake glucose

31 Glucagon Secretion promoted by:
Low plasma [glucose] (< 100 mg/dL) Increased plasma amino acids Sympathetic input Secretion inhibited by increased [glucose] Inhibition by insulin??

32 Glucagon Raises Plasma Glucose
Main purpose is to respond to hypoglycemia Activates enzymes for: Glycogenolysis – glycogen breakdown Gluconeogenesis – glucose synthesis

33 Response to Hypoglycemia in Fasted State
Figure 22-15

34 Diabetes Mellitus Family of diseases
Chronic elevated plasma glucose levels = hyperglycemia Two types: Type 1 – insulin deficiency Type 2 – ‘insulin-resistant’ diabetes; cells do not respond to insulin

35 Type 1 Diabetes ~10% of cases
Absorb nutrients normally, but no insulin released – what happens? Cells shift to fasted state, leading to glucose production! Results in hyperglycemia and cascading effects

36 Figure 22-16

37 Type 2 Diabetes ~90% of cases
Target cells do not respond normally to insulin Delayed response to ingested glucose Leads to hyperglycemia Often have elevated glucagon – why? No uptake of glucose by α cells Release glucagon Exercise and modified diet help treat – why?

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