Overnutrition, ectopic lipid and the metabolic syndrome

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

The metabolic syndrome is a constellation of metabolic risk factors including atherogenic dyslipidemia (elevated serum triglycerides, reduced high-density lipoprotein (HDL) cholesterol), elevated blood pressure, dysglycemia (insulin resistance and elevated serum glucose), a pro-inflammatory state, and a prothrombotic state. Most persons with metabolic syndrome are obese, and usually have abdominal obesity. Generally, obesity is a reflection of overnutrition. A current view is that when adipose tissue fails to store all excess nutrients as triglyceride, lipid begins to accumulate in various tissues (eg, muscle, liver, pancreas, and heart). This accumulation is called ectopic lipid. Various mechanisms have been proposed whereby ectopic lipid is detrimental in different tissues; these derangements induce metabolic risk factors. The foundation of the metabolic syndrome thus appears to be overnutrition, that is, more nutrient intake than can be safely disposed by lipid oxidation. Excess dietary carbohydrate also induces ectopic lipid. Of interest, less than half of obese individuals develop metabolic syndrome. Through various mechanisms they adapt to overnutrition so as to minimize lipid overload in tissues, and consequently, prevent the syndrome.

Original languageEnglish (US)
Pages (from-to)1082-1086
Number of pages5
JournalJournal of Investigative Medicine
Volume64
Issue number6
DOIs
StatePublished - Aug 1 2016

Fingerprint

Overnutrition
Lipids
Tissue
Nutrients
Triglycerides
Dietary Carbohydrates
Food
Abdominal Obesity
Blood pressure
Dyslipidemias
Serum
Liver
HDL Cholesterol
Muscle
Insulin Resistance
Adipose Tissue
Pancreas
Obesity
Insulin
Blood Pressure

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Overnutrition, ectopic lipid and the metabolic syndrome. / Grundy, Scott M.

In: Journal of Investigative Medicine, Vol. 64, No. 6, 01.08.2016, p. 1082-1086.

Research output: Contribution to journalReview article

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