Progesterone and Diabetes

Dr. Weeks’ Comment: Progesterone (the real stuff) is so named because it is “pro” “gestational” – it promotes gestation and protects the pregnancy through to term. This is in contrast to synthetic “knock offs” like medroxyprogesterone or Progestins which are hormone disrupters and deliver many bad side-effects. The real bioidentical progesterone has many benefits including: 1) lessening adrenalin (safer than a beta-blocker) 2) lessening anxiety (safer than a benzodiazepines or anxiolytic) 3) lessening the effect of estrogen 4) reducing osteoporosis via stimulating bone rebuilding (enhances osteoblasts) and 5) protection and regeneration of nervous tissues (neuroprotective and neuroregenerative) . What is paradoxical is how progesterone benefits diabetics – in part because it is anti-inflammatory and also because it induces hyperinsulinemia (delivers blood sugar into the cell and out of the circulation). Progesterone is also beneficial for weight loss as it promotes ketogenesis. The following articles help us paint an enticing picture.

Am J Obstet Gynecol. 1982 Mar 15;142(6 Pt 2):735-8.

Metabolic effects of progesterone.

Kalkhoff RK.


Progesterone has important effects on carbohydrate, lipid and protein metabolism. This steroid induces hyperinsulinemia, possibly by direct action on pancreatic islets, while promoting glycogen storage in the liver. Paradoxically, it antagonizes the effects of insulin on glucose metabolism in adipose tissue and skeletal muscle. Progesterone stimulates deposition of body fat but had catabolic effects on protein metabolism. Provisional evidence is offered that the steroid may influence ketone body production by the liver as well. When these steroid actions are considered together, their most relevant expression appears to be the physiologic changes observed during normal pregnancy.


Parenteral progesterone injections into different mammalian species induce hyperinsulinemia, pancreatic islet hypertrophy, and exaggerated insulin secretion in vitro in response to glucose. The primary effect of progesterone by itself on carbohydrate metabolism appears to be the diversion of glucose utilization away from muscle and fat to other tissues, and the promotion of more storage of glycogen in the liver. On lipid metabolism, the 1 effect of progesterone is to favor storage of depot fat in adipose and breast tissue and to partially reduce the hypertriglyceridemic action of estrogens. On protein metabolism, it has been suggested that progesterone may have a catabolic action in man, and that the basic effects may be a lowering of several plasma amino acids and an increased total urinary nitrogen excretion without an associated aminoaciduria. On ketone body metabolism, progesterone partially suppresses the estrogen effect on liver triglyceride formation while promoting ketogenesis. The metabolic effects of progesterone are most relevant to pregnancy. The hormonal milieu of early to midgestation favors the stimulation of hyperphagia, pancreatic islet hypertrophy, hyperinsulinemia, and body fat and glycogen deposition. This period promotes maternal tissue accretion and weight gain. During the later half of pregnancy, progesterone acts simultaneously with prolactin and other hormones to prepare the breasts for lactation by promoting hyperinsulinemia and fuel storage and by helping to condition the liver in elaborating ketones more promptly to meet the demands of advancing pregnancy.

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