Children with obesity who follow a ketogenic diet for four months show lower fasting insulin levels, which is associated with better insulin sensitivity and a lower risk of conditions related to...
Mechanism
Synthesis from 1 study
Cutting carbs stops blood sugar spikes, so the pancreas makes less insulin. At the same time, the body burns fat and makes ketones, which help muscles and liver take in sugar better and reduce inflammation, so even less insulin is needed to keep blood sugar normal.
Most probable mechanism
When carbs are very low, blood sugar doesn't spike after meals, so the pancreas releases less insulin. At the same time, the body makes ketones from fat, which help muscle and liver cells take up sugar more efficiently and reduce inflammation, so the body needs even less insulin to keep blood sugar normal.
Carbohydrate intake is restricted to below 40 grams per day, eliminating postprandial glucose excursions
Reduced glucose excursions decrease stimulation of pancreatic beta cells, lowering insulin secretion
Hepatic fatty acid oxidation produces ketone bodies, primarily β-hydroxybutyrate
β-hydroxybutyrate activates the AKT/GSK3β pathway in skeletal muscle, increasing GLUT4 translocation and glucose uptake
β-hydroxybutyrate reduces hepatic diacylglycerol content and inhibits PKC-ε activity, improving liver insulin sensitivity
β-hydroxybutyrate activates GPR109A receptors on adipocytes, stimulating adiponectin synthesis
Adiponectin enhances insulin sensitivity in muscle and liver through AMPK and PPARα activation
β-hydroxybutyrate inhibits the NLRP3 inflammasome, reducing systemic inflammation and removing suppression of adiponectin secretion
Lower insulin levels reduce stimulation of ovarian theca cells, decreasing androgen synthesis and increasing sex hormone-binding globulin production
Reduced visceral adipose tissue decreases local cortisol regeneration by 11β-HSD1, lowering systemic cortisol
Lower cortisol and reduced inflammation attenuate HPA axis overactivation, further stabilizing metabolic homeostasis
Less supported by current evidence, but not ruled out
The body shifts from using sugar to using fat and ketones for energy, which reduces the conversion of the inactive thyroid hormone T4 into the active form T3 in the liver and kidneys, without changing the signal from the brain that controls the thyroid.
Metabolic shift to fat and ketone utilization mimics a fasting state
Type 1 deiodinase activity in liver and kidney is downregulated
Conversion of thyroxine (T4) to triiodothyronine (T3) decreases, lowering circulating T3 levels
Thyroid-stimulating hormone (TSH) remains unchanged due to intact hypothalamic-pituitary feedback
Evidence from Studies
Supporting (1)
Community contributions welcome
Low-Carbohydrate (Ketogenic) Diet in Children with Obesity: Part 2—Hormonal Effects of the Ketogenic Diet
Contradicting (0)
Community contributions welcome
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