A recent study published in the Journal Science Translational Medicine offers more evidence that propionic acid increases blood sugar by inducing glycogenolysis and compensatory hyperinsulinemia impairing insulin activity in the body.  This is a critical topic—fundamental to preventative health.

Propionic Acid Could be a Problem

Researchers found that long-term exposure of mice to daily low doses of propionate resulted in gradual weight gain and insulin resistance as well as high blood sugar. Why does this matter? Diabetes is a disease driven by blood sugar accumulation—producing dangerously high blood sugar levels.

Blood sugar, our main source of energy, originates from the foods we eat. It is regulated by insulin and therefore insulin resistance events increase blood sugar.  Glycogenolysis, a metabolic breakdown of glycogen to glucose and it may lad to increases blood sugar.   What follows is a summary of the study conducted by research institutions in the United States and Israel.

Abstract

The short-chain fatty acid propionate is a potent inhibitor of molds that is widely used as a food preservative and endogenously produced by gut microbiota. Although generally recognized safety by the US FDA, the metabolic effects of propionate consumption in humans is unclear.

The study authors report that propionate stimulates glycogenolysis and hyperglycemia in mice by increasing plasma concentrations of glucagon and fatty acid-binding protein 4 (FABP4). Fabp4-deficient mice and mice lacking liver glucagon receptor were protected from the effects of propionate.  Although propionate did not directly promote glucagon or FABP4 secretion in ex vivo rodent pancreatic islets and adipose tissue models, respectively, it activated the sympathetic nervous system in mice, leading to secretion of these hormones in vivo. This effect could be blocked by the pharmacological inhibition of norepinephrine, which prevented propionate-induced hyperglycemia in mice.

In a randomized, double-blind, placebo-controlled study in humans, consumption of a propionate-containing mixed meal resulting in a postprandial increase in plasma glucagon, FABP4, and norepinephrine, leading to insulin resistance and compensatory hyperinsulinemia. Chronic exposure of mice to a propionate dose equivalent to that used for food preservation resulted in gradual weight gain.

In humans, plasma propionate decreased with weight loss in the DIRECT (Dietary Intervention Randomized Controlled Trial) trial and served as an independent predictor of improved insulin sensitivity. Thus propionate may activate a catecholamine-mediated increase in insulin counter-regulatory signals, leading to insulin resistance and hyperinsulinemia, which over time may promote adiposity and metabolic abnormalities. The investigators recommend further evaluation of metabolic consequences of propionate consumption.

Authors/Research Institutions

  • Mir Tirosh, Dalia and David Arabov Endocrinology and Diabetes Research Center, Institute of Endocrinology, Sheba Medical Center, Tel-Hashomer, Israel.
  • Ediz S Calay, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA
  • Gurol Tuncman, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Kathryn C Claiborn, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Karen E. Inouye, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Kosei Eguchi, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Michael Alcala, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
  • Moran Rathuas, Dalia and David Arabov Endocrinology and Diabetes Research Center, Institute of Endocrinology, Sheba Medical Center, Tel-Hashomer, Israel.
  • Kenneth S. Hollander, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
  • Idit Ron, Dalia and David Arabov Endocrinology and Diabetes Research Center, Institute of Endocrinology, Sheba Medical Center, Tel-Hashomer, Israel.
  • Rinat Livne, Dalia and David Arabov Endocrinology and Diabetes Research Center, Institute of Endocrinology, Sheba Medical Center, Tel-Hashomer, Israel.
  • Yoriko Heianza, Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA
  • Lu Qi, Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, USA
  • Iris Shai, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
  • Rajesh Garg, Division of Endocrinology, Diabetes and Hypertension, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
  • Gökhan S. Hotamisligil, Department of Genetics and Complex Diseases & Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA, USA
Source: STM Sciencemag

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