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Carbohydrates, Insulin, and Obesity

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Dr. Scherger reports no financial relationships relevant to this field of study.

SOURCE : Astley CM, Todd JN, Salem RM, et al. Genetic evidence that carbohydrate-stimulated insulin secretion leads to obesity. Clin Chem 2018:64:192-200.

Astley et al used several large databases and meta-analyses to estimate the causal relationship between insulin secretion and body mass index (BMI). The data sources included summary results from the largest published studies of people from a predominately European ancestry for insulin secretion. Data also were drawn from the Cardiology and Metabolic Patient Cohort study at Massachusetts General Hospital to validate genetic associations with insulin secretion and to test the observational association of insulin with BMI.

Genetics is a partial determinant of insulin concentration in the blood 30 minutes after oral glucose, known as the insulin-30 index. In their research, Astley et al discovered that higher genetically determined insulin-30 was associated strongly with higher BMI consistent with a causal role in obesity.


Clinicians learn in medical school that the role of insulin is to drive glucose into cells so that it can be used for energy. That fundamental role is highlighted by the pathophysiology of type 1 diabetes. There are other important metabolic roles for insulin that become important in obesity and type 2 diabetes. Insulin causes fat storage (lipogenesis) and blocks the burning of fat (lipolysis). Insulin also increases hunger and lowers energy expenditure. 1

Insulin causes the human body to burn glucose rather than fat. Any circulating glucose not needed for energy becomes fat through lipogenesis. High insulin blood levels reflect a stress to metabolism to burn glucose for energy rather than fat. High insulin levels also cause inflammation. When insulin levels become low, the body will burn fat for energy, resulting in ketosis. Researchers have demonstrated that burning fat to a degree that...