Comprehensive Physiology Wiley Online Library

The Metabolic Actions of Growth Hormone

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Abstract

The sections in this article are:

1 Growth Hormone as a Metabolic Hormone
1.1 Historical Background
1.2 Growth Hormone and Insulin‐like Growth Factor 1
1.3 Biochemical Interrelationships: The Glucose‐Fatty Acid Cycle
2 Metabolic Effects of Growth Hormone as Revealed in Whole Body Studies
2.1 Chronic Long‐Term Effects
2.2 Short‐Term Effects of Growth Hormone as Studied in Vivo
3 Effects of Growth Hormone on Individual Target Tissues
3.1 Liver
3.2 Muscle
3.3 Adipose Tissue
3.4 Pancreatic Beta Cells
4 Unresolved Issues
4.1 Does Insulin‐like Growth Factor 1 Mediate the Metabolic Effects of Growth Hormone?
4.2 Growth Hormone and Insulin Sensitivity
4.3 Do All of the Responses to Growth Hormone Arise from a Single Interaction of Growth Hormone with Its Receptor?
4.4 Biological Activities of Growth Hormone Fragments
5 Summary, Conclusions, and Future Directions
Figure 1. Figure 1.

Inhibition of specific binding of [125I]‐hGH to rat epididymal adipocytes by polyclonal antiserum raised against the extracellular domain of the rat GH receptor.

[Antiserum provided by Dr. William Baumbach of American Cyanamid.]
Figure 2. Figure 2.

Metabolic pathways in rodent skeletal muscle. Allosteric regulatory effects of metabolites are shown by the shaded arrows. Unbroken arrows accompanied by a (+) sign denote stimulation. Dashed arrows accompanied by a (−) sign denote inhibition.

Figure 3. Figure 3.

Lipid storage and mobilization in adipocytes. R1 and R2 are receptors for agonists that stimulate lipolysis, and R3 and R4 denote inhibitory receptors. Gs and Gi are the stimulatory and inhibitory guanine nucleotide‐binding proteins, respectively. AC = adenylyl clyclase, PDE = cyclic nucleotide phosphodiesterase. PKA = protein kinase A, PKA* = activated protein kinase A, HSL = hormone‐sensitive lipase and HSL* = activated hormone‐sensitive lipase. LPL = lipoprotein lipase, VLDL = very low density lipoproteins, FFA plasma free fatty acids. Intracellular fatty acids may arise from breakdown of adipocyte triglycerides, plasma VLDL, or de novo synthesis from glucose. Glycerol released by lipolysis of triglycerides cannot be reutilized for triglyceride synthesis, which requires α‐glycerol phosphate that arises from glucose metabolism.

Figure 4. Figure 4.

Autoradiogram of 32P‐labeled G‐proteins from rat epididymal adipocytes after separation by polyacrylamide gel electrophoresis. Adipocyte extracts were prepared from normal, hypophysectomized, and hypophysectomized rats treated with GH 4 h earlier. The extracts were incubated either with (32P)NAD+ in the presence of cholera toxin to label the alpha subunit of Gs or with a mixture of cholera toxin and pertussis toxin (ptx) to label the alpha subunits of both Gs and Gi. The abundance of NAD ribosylated Gsα, which migrated on the gel as two bands, was similar in all three conditions, but hypophysectomy selectively increased Giα, which migrated as a single band. Treatment with GH partially reversed the effect of hypophysectomy on Giα.

Figure 5. Figure 5.

Panel A: traditional view of the balance between inhibitory and stimulatory influences on the activity of adenylate cyclase. Panel B: modulation of the relative stimulatory and inhibitory inputs by resting the balance beam on a movable fulcrum. Growth hormone can be viewed as applying leftward pressure on the handle, thereby moving the fulcrum leftward and diminishing inhibitory input.

(From Goodman et al., with permission.)


Figure 1.

Inhibition of specific binding of [125I]‐hGH to rat epididymal adipocytes by polyclonal antiserum raised against the extracellular domain of the rat GH receptor.

[Antiserum provided by Dr. William Baumbach of American Cyanamid.]


Figure 2.

Metabolic pathways in rodent skeletal muscle. Allosteric regulatory effects of metabolites are shown by the shaded arrows. Unbroken arrows accompanied by a (+) sign denote stimulation. Dashed arrows accompanied by a (−) sign denote inhibition.



Figure 3.

Lipid storage and mobilization in adipocytes. R1 and R2 are receptors for agonists that stimulate lipolysis, and R3 and R4 denote inhibitory receptors. Gs and Gi are the stimulatory and inhibitory guanine nucleotide‐binding proteins, respectively. AC = adenylyl clyclase, PDE = cyclic nucleotide phosphodiesterase. PKA = protein kinase A, PKA* = activated protein kinase A, HSL = hormone‐sensitive lipase and HSL* = activated hormone‐sensitive lipase. LPL = lipoprotein lipase, VLDL = very low density lipoproteins, FFA plasma free fatty acids. Intracellular fatty acids may arise from breakdown of adipocyte triglycerides, plasma VLDL, or de novo synthesis from glucose. Glycerol released by lipolysis of triglycerides cannot be reutilized for triglyceride synthesis, which requires α‐glycerol phosphate that arises from glucose metabolism.



Figure 4.

Autoradiogram of 32P‐labeled G‐proteins from rat epididymal adipocytes after separation by polyacrylamide gel electrophoresis. Adipocyte extracts were prepared from normal, hypophysectomized, and hypophysectomized rats treated with GH 4 h earlier. The extracts were incubated either with (32P)NAD+ in the presence of cholera toxin to label the alpha subunit of Gs or with a mixture of cholera toxin and pertussis toxin (ptx) to label the alpha subunits of both Gs and Gi. The abundance of NAD ribosylated Gsα, which migrated on the gel as two bands, was similar in all three conditions, but hypophysectomy selectively increased Giα, which migrated as a single band. Treatment with GH partially reversed the effect of hypophysectomy on Giα.



Figure 5.

Panel A: traditional view of the balance between inhibitory and stimulatory influences on the activity of adenylate cyclase. Panel B: modulation of the relative stimulatory and inhibitory inputs by resting the balance beam on a movable fulcrum. Growth hormone can be viewed as applying leftward pressure on the handle, thereby moving the fulcrum leftward and diminishing inhibitory input.

(From Goodman et al., with permission.)
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How to Cite

H. Maurice Goodman. The Metabolic Actions of Growth Hormone. Compr Physiol 2011, Supplement 21: Handbook of Physiology, The Endocrine System, The Endocrine Pancreas and Regulation of Metabolism: 849-906. First published in print 2001. doi: 10.1002/cphy.cp070228