Visceral adiposity and metabolic syndrome after very high–fat and low-fat isocaloric diets: a randomized controlled trial1,2

  1. Gunnar Mellgren3,4,6,*
  1. 3Department of Clinical Science,
  2. 4KG Jebsen Centre for Diabetes Research, Department of Clinical Science, and
  3. 5Department of Clinical Medicine, University of Bergen, Bergen, Norway; and
  4. 6Hormone Laboratory and
  5. 7Department of Heart Disease, Haukeland University Hospital, Bergen, Norway
  1. *To whom correspondence should be addressed. E-mail: simon.dankel{at}uib.no (SN Dankel), gunnar.mellgren{at}uib.no (G Mellgren).
  • 1 This work was supported by the Western Norway Regional Health Authority, Meltzerfondet, Bergen Medical Research Foundation, and the University of Bergen. The following companies in Norway provided some of the products used in the study: Au Naturel (United Kingdom), Inc., Oslo (Solaray Spektro multivitamin and mineral supplement without iron), Tine ASA, Bergen (butter), Soma Nordic AS, Moss (Cocosa coconut oil), and Funksjonell Mat AS, Oslo (Sukrin+, a sugar substitute containing erythritol and stevia, a special mix with almond flour and plant fibers for making low-carbohydrate breads and cakes). Dietika AS, Drammen, Norway, provided discounted use of the online dietary registration tool at www.diett.no.

  • 2 Supplemental Tables 1–8 and Supplemental Figure 1 are available from the “Online Supporting Material” link in the online posting of the article and from the same link in the online table of contents at http://ajcn.nutrition.org.

  • 8 These authors were cofirst authors for this work.

Abstract

Background: Different aspects of dietary pattern, including macronutrient and food profiles, may affect visceral fat mass and metabolic syndrome.

Objective: We hypothesized that consuming energy primarily from carbohydrate or fat in diets with similar food profiles would differentially affect the ability to reverse visceral adiposity and metabolic syndrome.

Design: Forty-six men (aged 30–50 y) with body mass index (in kg/m2) >29 and waist circumference >98 cm were randomly assigned to a very high–fat, low-carbohydrate (VHFLC; 73% of energy fat and 10% of energy carbohydrate) or low-fat, high-carbohydrate (LFHC; 30% of energy fat and 53% of energy carbohydrate) diet for 12 wk. The diets were equal in energy (8750 kJ/d), protein (17% of energy), and food profile, emphasizing low-processed, lower-glycemic foods. Fat mass was quantified with computed tomography imaging.

Results: Recorded intake of carbohydrate and total and saturated fat in the LFHC and VHFLC groups were 51% and 11% of energy, 29% and 71% of energy, and 12% and 34% of energy, respectively, with no difference in protein and polyunsaturated fatty acids. Mean energy intake decreased by 22% and 14% in the LFHC and VHFLC groups. The diets similarly reduced waist circumference (11–13 cm), abdominal subcutaneous fat mass (1650–1850 cm3), visceral fat mass (1350–1650 cm3), and total body weight (11–12 kg). Both groups improved dyslipidemia, with reduced circulating triglycerides, but showed differential responses in total and low-density lipoprotein cholesterol (decreased in LFHC group only), and high-density lipoprotein cholesterol (increased in VHFLC group only). The groups showed similar reductions in insulin, insulin C-peptide, glycated hemoglobin, and homeostasis model assessment of insulin resistance. Notably, improvements in circulating metabolic markers in the VHFLC group mainly were observed first after 8 wk, in contrast to more acute and gradual effects in the LFHC group.

Conclusions: Consuming energy primarily as carbohydrate or fat for 3 mo did not differentially influence visceral fat and metabolic syndrome in a low-processed, lower-glycemic dietary context. Our data do not support the idea that dietary fat per se promotes ectopic adiposity and cardiometabolic syndrome in humans. This study was registered at clinicaltrials.gov as NCT01750021.

Keywords:
  • Received September 22, 2015.
  • Accepted October 28, 2016.

This Article

  1. Am J Clin Nutr
    ajcn123463
  1. Online Supporting Material
  2. All Versions of this Article:
    1. ajcn.115.123463v1
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