Role of insulin and other related hormones in energy metabolism—A review

Figures & data

Figure 1. Histological structure of pancreas (Longnecker, 2014).

Figure 2. Blood sugar insulin cycle graphic (Winter, 2013).

Table 1. Metabolic effects of hormones (Marilou, 2004)

Pathway	Insulin	Glucagon	Epinepherin	T3, T4	Cortisol	Growth hormone
Glycolysis	(+)	(−)	(+)	(+)	(−)	(−)
Glycogenesis	(+)	(−)	(−)	(−)	(+)	(+)
Glycogenolysis	(−)	(+) “Liver”	(+) “L&M”	(+)	(−)	(+)
Gluconeogenesis	(−)	(+)	(+)	(+)	(+)	(+)
Lipogenesis	(+)	(−)	(−)	(−)	(+) “central”	(−)
Lipolysis	(−)	(+)	(+)	(+)	(+) “peripheral”	(+)
Protein synthesis	(+)	(−)	(−)	(+)	(+)	(++)
Proteolysis	(−)	(+)

Notes: (+) stimulated, (−) inhibited.

Table 2. Mechanism of action of key metabolic regulators (Shrayyef & Gerich, 2010)

Hormones	Glucose production	Glucose utilization	Lipolysis
Insulin	Decrease	Increase	Decrease
Gucagon	Increase	–	–
Epinepherine	Increase	Decrease	Increase
Cortisol	Increase	Decrease	Increase
Growth hormone	Increase	Decrease	Increase
Free fatty acids	Increase	Decrease	–

Figure 3. Actions of insulin (Martin, 1983).

Figure 4. Utilization of glucose in metabolic specialization organs and cells (McKee & McKee, 2012b).

Figure 5. Role of insulin and glucagon in glucose regulation (Rajendran, Pharm, & Santhi, 1979).

Figure 6. Role of insulin and glucagon in metabolic processes of carbohydrates (Dashty, 2013; McKee & McKee, 2012b).

Figure 7. Cori cycle (Dashty, 2013).

Figure 8. Regulation of fatty acid synthesis (McKee & McKee, 2012c).

Figure 9. Overview of the randle cycle (the glucose/fatty acid cycle) (Dimitriadis et al., 2011).

Table 3. Factors and conditions increased and decreased insulin and glucagon secretion (Bassett, 1972, 1974; Evans, Buchanan-Smith, & Macleod, 1975; Ross & Kitts, 1973)

Insulin secretion		Glucagon Secretion
Increase	Decrease	Increase	Decrease
Postprandial	Blood glucose	Exercise and stress	Somatostatin
Blood glucose, FFA & AAs	Fasting	Gastrin & CCK	Insulin
GIH (gastrin, choleccystokinin, secretin, gastric inhibitory peptide)	Somatostatin	Cortisol	FFA
Glucagon, GH, cortisol	α–adrenergic activity	Epinephrine	Ketones
Parasympathetic stimulation	Epinephrine	Increase blood AA & VFA	Postprandial
Insulin resistance; obesity and VFAs			Increased blood glucose Atropine

Notes: AA: amino acids; FA: fatty acids; FFA: free fatty acids; CCK: Cholecystokinin; VVA: volatile fatty acids; GH: growth hormone; GIH: gastrointestinal hormones.

Table 4. Summary of metabolic effects of somatotrophin (Squires, 2011)

Tissue type	Metabolic effect
Skeletal muscle	Increased protein synthesis/accretion
Adipose tissue	Increased lipolysis, decreased glucose uptake and lipid synthesis
Liver	Increased glucose output
Intestine	Increased calcium and phosphorus uptake
Mammary gland	Increased milk synthesis by increased uptake of nutrients and increased blood flow
Various tissues	Decreased AA^* and glucose oxidation; increased oxidation of FFAs acids; decreased effects of insulin

Notes: AA: amino acids; FA: fatty acids; FFAs: free fatty acids.

Table 5. Hormones involved in regulation of blood glucose and their metabolic effect & actions (Rajendran et al., 1979)

Hormone	Action	Tissue of Origin	Metabolic effect	Effect on blood glucose
Insulin	It regulates the metabolism of carbohydrates and fats by promoting the absorption of glucose from the blood to skeletal muscles and fat tissue and by causing fat to be stored rather than used for energy	Pancreatic β cells	Enhances entry of glucose into cells; Enhances storage of glucose as glycogen, or conversion to FA; Enhances synthesis of FA and proteins; Suppresses breakdown of proteins into AA, of adipose tissue into FFA	Lowers
Glucagon	It produced when the glucose levels falls which raises glucose level in the bloodstream. Its effect is opposite that of insulin, which lowers the glucose concentration. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream	Pancreatic α cells	Enhances release of glucose from glycogen; Enhances synthesis of glucose from amino acids or fatty acids	Raises
Somatostatin	Inhibition of the release of numerous secondary hormones. It’s inhibits insulin and glucagon secretion	Pancreatic δ cells	Suppresses glucagon release from α cells (acts locally); suppresses release of Insulin, PTH, gastrin & secretin	Lowers
Epinephrine	It plays an important role in the fight-or-flight response by increasing blood flow to muscles, output of the heart, pupil dilation, and blood sugar	Adrenal medulla & neurons	Enhances release of glucose from glycogen; Enhances release of FA from adipose tissue	Raises
Cortisol	It is released in response to stress and low blood-glucose concentration	Adrenal cortex	Enhances gluconeogenesis; Antagonizes insulin	Raises
ACTH	ACTH acts on the adrenal cortex to promote glucocorticoid secretion (cortisol in humans). Hyperglycemic hormones such as glucagon	Anterior pituitary	Enhances release of cortisol; Enhances release of FAs from adipose tissue	Raises
Growth hormone (Somatotrophs)	Reduction in the blood glucose level and promotes secretion of GH from the pituitary gland through the hypothalamus	Anterior pituitary	Antagonizes insulin and somatostatin	Raises
Thyroxin	Act on metabolism, growth and development	Thyroid	Enhances release of glucose from glycogen; enhances absorption of sugars from intestine	Raises

Notes: AA: amino acids; FA: fatty acids; FFAs: free fatty acids; GH: growth hormone; PTH; Pituitary tropic hormones; ACTH: Adrenocorticotropic hormone.

Figure 10. Action and metabolic effect of somatostatin on insulin and glucagon (Rajendran et al., 1979).

Figure 11. Regulation of blood glucose level by insulin and glucagon and other related hormones (Rajendran et al., 1979).

Figure 12. Role of cortisol in converted protein and fat to glucose blood glucose in stress (Rajendran et al., 1979).

Figure 13. Metabolic disorder during stress (Marilou, 2004).

Figure 14. Glucose counter-regulatory hormones: effect on liver (Rajendran et al., 1979).

Figure 15. Metabolic effects of β-adrenergic agonists (Squires, 2011).

Figure 16. Regulation of growth hormone release (Squires, 2011).

Figure 17. Effects of thyroid hormones on metabolism, growth and development. BMR, basal metabolic rate (Squires, 2011).

Figure 18. Metabolic effects of leptin (Squires, 2011).

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