Insulin is a hormone that increases when blood glucose rises, and acts to reduce blood glucose by putting it into cells and increasing its usage. It temporarily shifts energy metabolism from fats to carbs, and does not inherently make somebody fat. Its potency is seen as Insulin Sensitivity.

This page features 106 unique references to scientific papers.

Research analysis by and verified by the Research Team. Last updated on Apr 29, 2017.

Summary of Insulin

Primary Information, Benefits, Effects, and Important Facts

Insulin is a hormone in the body secreted from the Pancreas, and is known as the Master regulator of carbohydrate metabolism. It works in concert with its sister hormone, Glucagon, and a host of other hormones to regulate blood sugar levels in the body and protect from an excess of blood sugar (hyperglycemia) or too low a level of blood sugar (hypoglycemia).

It is mostly an anabolic hormone, meaning it acts to build molecules and tissues. It has some catabolic properties though (catabolis as in acting to destroy molecules and tissues to provide energy).

When active, insulin and the actions of the proteins under its control can be summed up with having two main actions:

  • Causing a flux of nutrients into the liver, fat, and muscle; to get said nutrients out of the blood

  • Causing a metabolic shift towards carbohydrates, favoring them as fuel, and thus minimizing usage of both fats and proteins for energy

It is increased in response to the diet. Most notably carbohydrates and the a lesser extent proteins. In contrast to many hormones, Insulin is one that is highly responsive to diet and lifestyle; manipulating insulin levels through one's diet and lifestyle is common in diet strategies.

It is essential to survival, and those who do not produce any or insufficient levels of insulin must inject it otherwise (Type I Diabetics).

Insulin has a phenomena known as 'Insulin Sensitivity' which can be summed up as 'The amount of action a single molecule of insulin can exert inside a cell'. The more insulin sensitivity you have, the less overall insulin you need to exert the same effect. A large scale and prolonged state of insulin insensitivity is what is known as Type II diabetes (among other co-morbidities).

Insulin is neither bad nor good from a health and body composition perspective. It has certain roles in the body and activating it may or may not be beneficial for particular individuals, but may also be wondrous for others. Typically sedentary obese persons would be wise to limit insulin secretion while power athletes or relatively lean athletic individuals would be wise to use carbohydrate timing strategies to maximize the effects of insulin.

Editors' Thoughts on Insulin

Disregard this page until further notice, those who stumbled upon it in its infancy ;)

Not much info here

Kurtis Frank

Frequently Asked Questions

Questions and answers regarding Insulin

Q: Do artificial sweeteners spike insulin?

Read full answer to "Do artificial sweeteners spike insulin?"

Q: How are carbohydrates converted into fat deposits?

Read full answer to "How are carbohydrates converted into fat deposits?"

Q: Does dairy cause acne?

A: Growth factors can cause acne, either androgens or anything acting on the insulin receptor (including IGF-1) that enhance androgen signaling. Dairy is currently weakly suspected to contribute via the above, but not enough evidence exists to support a strong relationship.

Read full answer to "Does dairy cause acne?"

Q: How do I increase insulin sensitivity?

A: Exercise frequently (resistance training and aerobic training are both beneficial), eat better (in this regard, less processed carbohydrates and more vegetables), and lose weight. Supplements can help, but are better when the diet and exercise are in order

Read full answer to "How do I increase insulin sensitivity?"

Q: Low-fat vs low-carb? Major study concludes: it doesn’t matter for weight loss

A: A year-long randomized clinical trial has found that a low-fat diet and a low-carb diet produced similar weight loss and improvements in metabolic health markers. Furthermore, insulin production and tested genes had no impact on predicting weight loss success or failure. Thus, you should choose your diet based on personal preferences, health goals, and sustainability.

Read full answer to "Low-fat vs low-carb? Major study concludes: it doesn’t matter for weight loss"

Human Effect Matrix

The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what supplements affect insulin

Grade Level of Evidence
Robust research conducted with repeated double-blind clinical trials
Multiple studies where at least two are double-blind and placebo controlled
Single double-blind study or multiple cohort studies
Uncontrolled or observational studies only
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Outcome Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
All comparative evidence is now gathered in our ​Supplement Goals Reference.
The evidence for each separate supplement is still freely available ​here.
Salacia reticulata  
Vitamin B3 (Niacin)  
Whey Protein  
Cocoa Extract  
Conjugated Linoleic Acid  
Fish Oil  
Chlorogenic Acid  
Gynostemma pentaphyllum  
Olive leaf extract  
Black Cohosh  
Branched Chain Amino Acids  
Coenzyme Q10  
Gamma Oryzanol  
Green Tea Catechins  
Japanese Knotweed  
Krill Oil  
Panax ginseng  
Punicic Acid  
Red Clover Extract  
Rose Hip  
Sodium Bicarbonate  
Tauroursodeoxycholic Acid  
Ursolic Acid  
Vitamin D  
Vitamin E  
Vitamin K  
Mangifera indica  
Medium-chain triglycerides  
Safflower Oil  
Salvia hispanica  

Background information on the Hormone


mRNA encodes for a polypeptide chain known as Preproinsulin, which then passively folds into, via amino acid affinity, Insulin.[1]

Insulin is a peptide hormone (hormone made from amino acids) that is composed of two chains, an alpha chain 21 amino acids in length and a beta chain 30 amino acids in length.[2][1] It is connected by sulfide bridges between chains (A7-B7, A20-B19) and in the alpha chain (A6-A11)[1], which give it a hydrophobic core.[3]

This tertiary protein structure can exist by itself as a monomer[4], together with another as a dimer[5], and as a hexamer.[6]

These forms of insulin are metabolically inert[7] and become active when conformational (structural) changes occur when binding to the insulin receptor.[1]

Roles in the Body

In vivo synthesis, degradation, and regulation

Insulin is synthesized in the Pancreas, in a subset of the Pancreas[8] known as the 'Islets of Langerhans' exists beta-cells which are the sole producers of insulin.[9]

Insulin, after its synthesis, is released into the blood.

Once done its job, it is degraded by Insulin Degrading Enzyme (Insulysin)[10], which is ubiquitously expressed[11] and declines with age[12].

The insulin receptor signalling cascade

For simplicity, select intermediates that hold a critical spot in the signalling cascade have been bolded.

Insulin stimulation works via insulin acting on the outer side of the insulin receptor (which is embedded in the cell membrane, exposed to both the outside and inside), and causing structural (Conformational) changes that induce a tyrosine kinase on the inside portion of the receptor, and multiple phosphorylations.[13] The compounds that are directly phosphorylated by the inside portion of the insulin receptor include the four denoted substrates (Insulin Receptor Substrate, IRS, 1-4) as well as some other proteins known as Gab1, Shc, Cbl, APD, and SIRPs.[13] Phosphorylation of these intermediates causes structural changes to them that start the post-receptor signalling cascade.

PI3K (activated through the IRS1-4 intermediate) is sometimes seen as the main second tier intermediate[14] and acts through phosphoinositides to activate an intermediate known as Akt, which has its activity highly correlated with GLUT4 translocation.[15] Inhibition of PI3k by wortmannin completely abolishes insulin-mediated glucose uptake, suggesting the criticality of this pathway.[16]

GLUT4 translocation (the ability to take sugars into a cell) seems to be co-dependent on both PI3K activation (as stated above) as well as a CAP/Cbl cascade.[17][18] Activation of PI3K in vitro is not sufficient to explain all of insulin-mediated glucose uptake.[19][20] Activation of the primary intermediate APS recruits both CAP and c-Cbl to the insulin receptor where the form a dimer complex (bind together)[21][22] and then travel via lipid rafts[23] to GLUT4 vesicles, and via a GTP binding protein facilitate their movement to the cell surface.[24]

For a visual representation of the above, please refer to the KEGG metabolic pathway for insulin.

Effects on Carbohydrate Metabolism

Insulin is the main metabolic regulator of blood glucose (also known as blood sugar) levels. It acts in concert with its sister hormone Glucagon to balance blood glucose levels in the body. Insulin has both roles that increase and decrease glucose levels in the blood, namely by increasing synthesis of glucose and increasing deposition of glucose into cells; both anabolic (tissue-building) reactions which are generally in opposition to glucagons catabolic (tissue-destroying) actions.

Regulation of Glucose synthesis and degradation

Glucose can be generated from non-glucose sources in the liver and kidneys.[25] The kidneys tend to resorb approximately as much glucose as they synthesis however, indicating that they may be self-sustaining. This is the reason why the liver is seen as the main centre for gluconeogenesis (gluco = glucose, neo = new, genesis = create; to create new glucose).[26]

Insulin is secreted from the pancreas, and does so in response to when beta-cells detect rising glucose levels in the blood.[27] There are also neural sensors which can work vicariously through the pancreas.[28][29] When sugar in the blood rises, insulin (and other factors) mediate a systemic (whole-body) flux of glucose out of the blood and into the liver and other tissues (such as fat and muscle). Sugar can flux into and out of the liver via GLUT2, and is fairly independent of hormonal regulation[30] although some exists in the gut GLUT2.[31] In particular, the sensation of sweetness can upregulate GLUT2 activity in the gut.[32] The flux of glucose into the liver hinders creation of more glucose, and begins to favor production of glycogen via hepatic glycogenesis (glyco = glycogen, genesis = create; to create glycogen).[33][34]

Glucose Uptake into cells

Insulin acts to deliver glucose from the blood into muscle and fat cells via the transport known as GLUT4.[35] There are 6 GLUTs in the body (1-7, in which 6 is a pseudogene) but GLUT4 is the most commonly expressed and significant for muscle and fat tissue[35][13] and GLUT5 responding to fructose.[36]

GLUT4 is not a surface transport, but is contained in small vesicles inside the cell.[37] These vesicles can be moved to the surface of the cell (cytoplasmic membrane) by either insulin stimulation[38] of its receptor or by calcium release from the sarcoplasmic reticulum (muscle contraction).[39]

As mentioned earlier, a synergy of PI3K activation (via insulin signalling) and CAP/Cbl signalling (partially via insulin) is required for effective GLUT4 mobilization and uptake of glucose into fat and muscle cells (where GLUT4 is most commonly expressed).

Effects on Fat Metabolism

Effects on Protein Metabolism

Insulin Sensitivity and Resistance

Insulin resistance is also seen in high-fat diets (typically 60% total calories or greater), which may be due to adverse interactions with the CAP/Cbl signalling cascade required for GLUT4 translocation,[40][41] as the actual insulin receptor phosphorylation is unaffected and the phosphorylation of IRS intermediates only slightly adversed affected.[42]

Scientific Support & Reference Citations


  1. Hua Q. Insulin: a small protein with a long journey. Protein Cell. (2010)
  2. Bentley G, et al. Structure of insulin in 4-zinc insulin. Nature. (1976)
  3. Thermodynamics of the Hydrophobicity in Crystallization of Insulin.
  4. Bocian W, et al. Structure of human insulin monomer in water/acetonitrile solution. J Biomol NMR. (2008)
  5. Ganim Z, Jones KC, Tokmakoff A. Insulin dimer dissociation and unfolding revealed by amide I two-dimensional infrared spectroscopy. Phys Chem Chem Phys. (2010)
  6. Dodson G, Steiner D. The role of assembly in insulin's biosynthesis. Curr Opin Struct Biol. (1998)
  7. Liang DC, et al. The possible mechanism of binding interaction of insulin molecule with its receptor. Sci China B. (1992)
  8. Seymour PA, Sander M. Historical perspective: beginnings of the beta-cell: current perspectives in beta-cell development. Diabetes. (2011)
  9. Murtaugh LC. Pancreas and beta-cell development: from the actual to the possible. Development. (2007)
  10. Fernández-Gamba A, et al. Insulin-degrading enzyme: structure-function relationship and its possible roles in health and disease. Curr Pharm Des. (2009)
  11. Insulin-degrading enzyme is differentially expressed and developmentally regulated in various rat tissues.
  12. The effect of age on insulin-degrading activity in rat tissue.
  13. Watson RT, Pessin JE. Intracellular organization of insulin signaling and GLUT4 translocation. Recent Prog Horm Res. (2001)
  14. Phosphoinositide 3-kinase: the key switch mechanism in insulin signalling.
  15. Corvera S, Czech MP. Direct targets of phosphoinositide 3-kinase products in membrane traffic and signal transduction. Trends Cell Biol. (1998)
  16. The Effects of Wortmannin on Rat Skeletal Muscle.
  17. Saltiel AR, Pessin JE. Insulin signaling pathways in time and space. Trends Cell Biol. (2002)
  18. Khan AH, Pessin JE. Insulin regulation of glucose uptake: a complex interplay of intracellular signalling pathways. Diabetologia. (2002)
  19. The inability of phosphatidylinositol 3-kinase activation to stimulate GLUT4 translocation indicates additional signaling pathways are required for insulin-stimulated glucose uptake.
  20. Platelet-derived Growth Factor Inhibits Insulin Stimulation of Insulin Receptor Substrate-1-associated Phosphatidylinositol 3-Kinase in 3T3-L1 Adipocytes without Affecting Glucose Transport.
  21. A Novel, Multifunctional c-Cbl Binding Protein in Insulin Receptor Signaling in 3T3-L1 Adipocytes.
  22. The Roles of Cbl-b and c-Cbl in Insulin-stimulated Glucose Transport.
  23. Baumann CA, et al. CAP defines a second signalling pathway required for insulin-stimulated glucose transport. Nature. (2000)
  24. The TC10-interacting protein CIP4/2 is required for insulin-stimulated Glut4 translocation in 3T3L1 adipocytes.
  25. Cherrington AD. Banting Lecture 1997. Control of glucose uptake and release by the liver in vivo. Diabetes. (1999)
  26. Barthel A, Schmoll D. Novel concepts in insulin regulation of hepatic gluconeogenesis. Am J Physiol Endocrinol Metab. (2003)
  27. Palerm CC. Physiologic insulin delivery with insulin feedback: a control systems perspective. Comput Methods Programs Biomed. (2011)
  28. Thorens B. Brain glucose sensing and neural regulation of insulin and glucagon secretion. Diabetes Obes Metab. (2011)
  29. Klip A, Hawkins M. Desperately seeking sugar: glial cells as hypoglycemia sensors. J Clin Invest. (2005)
  30. Leturque A, Brot-Laroche E, Le Gall M. GLUT2 mutations, translocation, and receptor function in diet sugar managing. Am J Physiol Endocrinol Metab. (2009)
  31. Kellett GL, et al. Sugar absorption in the intestine: the role of GLUT2. Annu Rev Nutr. (2008)
  32. Mace OJ, et al. Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2. J Physiol. (2007)
  33. Nordlie RC, Foster JD, Lange AJ. Regulation of glucose production by the liver. Annu Rev Nutr. (1999)
  34. Radziuk J, Pye S. Hepatic glucose uptake, gluconeogenesis and the regulation of glycogen synthesis. Diabetes Metab Res Rev. (2001)
  35. James DE, Strube M, Mueckler M. Molecular cloning and characterization of an insulin-regulatable glucose transporter. Nature. (1989)
  36. Douard V, Ferraris RP. Regulation of the fructose transporter GLUT5 in health and disease. Am J Physiol Endocrinol Metab. (2008)
  37. Intracellular organization of insulin signaling and GLUT4 translocation.
  38. Thurmond DC, Pessin JE. Molecular machinery involved in the insulin-regulated fusion of GLUT4-containing vesicles with the plasma membrane (review). Mol Membr Biol. (2001)
  39. Jessen N, Goodyear LJ. Contraction signaling to glucose transport in skeletal muscle. J Appl Physiol. (2005)
  40. Singh MK, et al. High-fat diet and leptin treatment alter skeletal muscle insulin-stimulated phosphatidylinositol 3-kinase activity and glucose transport. Metabolism. (2003)
  41. Resistance training enhances components of the insulin signaling cascade in normal and high-fat-fed rodent skeletal muscle.
  42. Bernard JR, et al. High-fat feeding effects on components of the CAP/Cbl signaling cascade in Sprague-Dawley rat skeletal muscle. Metabolism. (2006)

Via HEM and FAQ:

  1. Spiers PA, et al. Aspartame: neuropsychologic and neurophysiologic evaluation of acute and chronic effects. Am J Clin Nutr. (1998)
  2. Ford HE, et al. Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects. Eur J Clin Nutr. (2011)
  3. Ma J, et al. Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. Am J Physiol Gastrointest Liver Physiol. (2009)
  4. Anton SD, et al. Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels. Appetite. (2010)
  5. Steinert RE, et al. Effects of carbohydrate sugars and artificial sweeteners on appetite and the secretion of gastrointestinal satiety peptides. Br J Nutr. (2011)
  6. Møller SE. Effect of aspartame and protein, administered in phenylalanine-equivalent doses, on plasma neutral amino acids, aspartate, insulin and glucose in man. Pharmacol Toxicol. (1991)
  7. Wolf-Novak LC, et al. Aspartame ingestion with and without carbohydrate in phenylketonuric and normal subjects: effect on plasma concentrations of amino acids, glucose, and insulin. Metabolism. (1990)
  8. Horwitz DL, McLane M, Kobe P. Response to single dose of aspartame or saccharin by NIDDM patients. Diabetes Care. (1988)
  9. Teff KL, Devine J, Engelman K. Sweet taste: effect on cephalic phase insulin release in men. Physiol Behav. (1995)
  10. Malaisse WJ, et al. Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets. Cell Signal. (1998)
  11. Andrew G. Renwicka,Samuel V. Molinarya. Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release. British Journal of Nutrition. (2010)
  12. Acheson KJ, et al. Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. Am J Clin Nutr. (1988)
  13. McDevitt RM, et al. De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. Am J Clin Nutr. (2001)
  14. Minehira K, et al. Effect of carbohydrate overfeeding on whole body and adipose tissue metabolism in humans. Obes Res. (2003)
  15. ROBINSON HM. The acne problem. South Med J. (1949)
  16. Melnik BC. Evidence for acne-promoting effects of milk and other insulinotropic dairy products. Nestle Nutr Workshop Ser Pediatr Program. (2011)
  17. Deplewski D, Rosenfield RL. Growth hormone and insulin-like growth factors have different effects on sebaceous cell growth and differentiation. Endocrinology. (1999)
  18. Aizawa H, Niimura M. Elevated serum insulin-like growth factor-1 (IGF-1) levels in women with postadolescent acne. J Dermatol. (1995)
  19. Cappel M, Mauger D, Thiboutot D. Correlation between serum levels of insulin-like growth factor 1, dehydroepiandrosterone sulfate, and dihydrotestosterone and acne lesion counts in adult women. Arch Dermatol. (2005)
  20. Hoppe C, et al. High intakes of skimmed milk, but not meat, increase serum IGF-I and IGFBP-3 in eight-year-old boys. Eur J Clin Nutr. (2004)
  21. Salehi A, et al. The insulinogenic effect of whey protein is partially mediated by a direct effect of amino acids and GIP on β-cells. Nutr Metab (Lond). (2012)
  22. Melnik BC. FoxO1 - the key for the pathogenesis and therapy of acne. J Dtsch Dermatol Ges. (2010)
  23. Kim SJ, et al. Glucose-dependent insulinotropic polypeptide (GIP) stimulation of pancreatic beta-cell survival is dependent upon phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signalling, inactivation of the forkhead transcription factor Foxo1, and down-regulation of bax expression. J Biol Chem. (2005)
  24. Melnik BC. Is nuclear deficiency of FoxO1 due to increased growth factor/PI3K/Akt-signalling in acne vulgaris reversed by isotretinoin treatment. Br J Dermatol. (2010)
  25. Melnik BC. The role of transcription factor FoxO1 in the pathogenesis of acne vulgaris and the mode of isotretinoin action. G Ital Dermatol Venereol. (2010)
  26. Makrantonaki E, Zouboulis CC. Testosterone metabolism to 5alpha-dihydrotestosterone and synthesis of sebaceous lipids is regulated by the peroxisome proliferator-activated receptor ligand linoleic acid in human sebocytes. Br J Dermatol. (2007)
  27. Smith TM, et al. IGF-1 induces SREBP-1 expression and lipogenesis in SEB-1 sebocytes via activation of the phosphoinositide 3-kinase/Akt pathway. J Invest Dermatol. (2008)
  28. Fan W, et al. Insulin-like growth factor 1/insulin signaling activates androgen signaling through direct interactions of Foxo1 with androgen receptor. J Biol Chem. (2007)
  29. Melnik B. {Acne vulgaris. Role of diet}. Hautarzt. (2010)
  30. Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. (2009)
  31. Bhate K, Williams HC. Epidemiology of acne vulgaris. Br J Dermatol. (2012)
  32. Danby FW. Acne and milk, the diet myth, and beyond. J Am Acad Dermatol. (2005)
  33. Adebamowo CA, et al. High school dietary dairy intake and teenage acne. J Am Acad Dermatol. (2005)
  34. Adebamowo CA, et al. Milk consumption and acne in teenaged boys. J Am Acad Dermatol. (2008)
  35. Meshkani R, Adeli K. Hepatic insulin resistance, metabolic syndrome and cardiovascular disease. Clin Biochem. (2009)
  36. Bastard JP, et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw. (2006)
  37. Cnop M, et al. Mechanisms of pancreatic beta-cell death in type 1 and type 2 diabetes: many differences, few similarities. Diabetes. (2005)
  38. Akirav E, Kushner JA, Herold KC. Beta-cell mass and type 1 diabetes: going, going, gone. Diabetes. (2008)
  39. Stecenko AA, Moran A. Update on cystic fibrosis-related diabetes. Curr Opin Pulm Med. (2010)
  40. Short KR, et al. Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity. Diabetes. (2003)
  41. Karakelides H, et al. Age, obesity, and sex effects on insulin sensitivity and skeletal muscle mitochondrial function. Diabetes. (2010)
  42. Finucane FM, et al. The effects of aerobic exercise on metabolic risk, insulin sensitivity and intrahepatic lipid in healthy older people from the Hertfordshire Cohort Study: a randomised controlled trial. Diabetologia. (2010)
  43. van der Heijden GJ, et al. Aerobic exercise increases peripheral and hepatic insulin sensitivity in sedentary adolescents. J Clin Endocrinol Metab. (2009)
  44. Goulet ED, et al. Aerobic training improves insulin sensitivity 72-120 h after the last exercise session in younger but not in older women. Eur J Appl Physiol. (2005)
  45. Winnick JJ, et al. Short-term aerobic exercise training in obese humans with type 2 diabetes mellitus improves whole-body insulin sensitivity through gains in peripheral, not hepatic insulin sensitivity. J Clin Endocrinol Metab. (2008)
  46. Krogh-Madsen R, et al. A 2-wk reduction of ambulatory activity attenuates peripheral insulin sensitivity. J Appl Physiol. (2010)
  47. Fisher G, Hunter GR, Gower BA. Aerobic exercise training conserves insulin sensitivity for 1 yr following weight loss in overweight women. J Appl Physiol. (2012)
  48. Nassis GP, et al. Aerobic exercise training improves insulin sensitivity without changes in body weight, body fat, adiponectin, and inflammatory markers in overweight and obese girls. Metabolism. (2005)
  49. Carr DB, et al. A reduced-fat diet and aerobic exercise in Japanese Americans with impaired glucose tolerance decreases intra-abdominal fat and improves insulin sensitivity but not beta-cell function. Diabetes. (2005)
  50. van der Heijden GJ, et al. A 12-week aerobic exercise program reduces hepatic fat accumulation and insulin resistance in obese, Hispanic adolescents. Obesity (Silver Spring). (2010)
  51. Van Der Heijden GJ, et al. Strength exercise improves muscle mass and hepatic insulin sensitivity in obese youth. Med Sci Sports Exerc. (2010)
  52. Black LE, Swan PD, Alvar BA. Effects of intensity and volume on insulin sensitivity during acute bouts of resistance training. J Strength Cond Res. (2010)
  53. Gardner CD, et al.. Effect of Low-Fat vs. Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association with Genotype Pattern or Insulin Secretion: The DIETFITS Randomized Clinical Trial. JAMA. (2018)
  54. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. (2007)
  55. Sacks FM, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med. (2009)
  56. Pittas AG, et al. A low-glycemic load diet facilitates greater weight loss in overweight adults with high insulin secretion but not in overweight adults with low insulin secretion in the CALERIE Trial. Diabetes Care. (2005)
  57. Qi Q, et al. Insulin receptor substrate 1 gene variation modifies insulin resistance response to weight-loss diets in a 2-year randomized trial: the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial. Circulation. (2011)
  58. Westman EC, et al. Low-carbohydrate nutrition and metabolism. Am J Clin Nutr. (2007)
  59. Hall KD, Guo J. Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology. (2017)
  60. Johnston BC, et al. Comparison of weight loss among named diet programs in overweight and obese adults: a meta-analysis. JAMA. (2014)
  61. Bueno NB, et al. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Br J Nutr. (2013)
  62. McClain AD, et al. Adherence to a low-fat vs. low-carbohydrate diet differs by insulin resistance status. Diabetes Obes Metab. (2013)
  63. Cornier MA, et al. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women. Obes Res. (2005)
  64. Jensen MD, et al. 2013 AHA/ACC/TOS guideline for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society. Circulation. (2014)