Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Aug;33(8):1817-22.
doi: 10.2337/dc10-0284.

Central role of fatty liver in the pathogenesis of insulin resistance in obese adolescents

Affiliations

Central role of fatty liver in the pathogenesis of insulin resistance in obese adolescents

Ebe D'Adamo et al. Diabetes Care. 2010 Aug.

Abstract

Objective: We evaluated the role of fatty liver in the alteration of insulin sensitivity and beta-cell function in two groups of obese adolescents, differing in hepatic fat content (hepatic fat fraction [HFF]) but with similar intrabdominal intramyocellular lipid content (IMCL) and overall degree of obesity.

Research design and methods: We studied 23 obese adolescents with high HFF (HFF >5.5%) and 20 obese adolescents with low HFF (HFF <5.5%), matched for age, Tanner stage, BMI z score, and percentages of body fat, visceral fat, and IMCL. All subjects underwent an oral glucose tolerance test and a two-step hyperinsulinemic-euglycemic clamp, magnetic resonance imaging and (1)H nuclear magnetic resonance to assess abdominal fat distribution, HFF, and IMCL, respectively.

Results: The high HFF group showed significantly lower whole-body insulin sensitivity index (P = 0.001) and estimates of insulin secretion (P = 0.03). The baseline hepatic glucose production (EGP) rate was not different between the two groups. Suppression of EGP was significantly lower (P = 0.04) in the high HFF group during low-dose insulin; no differences were observed during the second step. Baseline fatty acids, glycerol concentrations, and clamp suppression of glycerol turnover did not differ between the groups. During the second step, the glucose disposal rate was significantly lower (P = 0.01) in the high HFF group.

Conclusions: Fatty liver, independent of visceral fat and IMCL, plays a central role in the insulin-resistant state in obese adolescents.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Percent suppression of hepatic glucose production and lipolysis and muscle insulin sensitivity in low (■) and high (□) liver fat content groups, during the low- and high-dose insulin infusion.

References

    1. Schwimmer JB, Deutsch R, Kahen T, Lavine JE, Stanley C, Behling C: Prevalence of fatty liver in children and adolescents. Pediatrics 2006;118:1388–1393 - PubMed
    1. Cali AM, De Oliveira AM, Kim H, Chen S, Reyes-Mugica M, Escalera S, Dziura J, Taksali SE, Kursawe R, Shaw M, Savoye M, Pierpont B, Constable RT, Caprio S: Glucose dysregulation and hepatic steatosis in obese adolescents: is there a link? Hepatology 2009;49:1896–1903 - PMC - PubMed
    1. Taksali SE, Caprio S, Dziura J, Dufour S, Calí AM, Goodman TR, Papademetris X, Burgert TS, Pierpont BM, Savoye M, Shaw M, Seyal AA, Weiss R: High visceral and low abdominal subcutaneous fat stores in the obese adolescent. Diabetes 2008;57:367–371 - PubMed
    1. Bacha F, Saad R, Gungor N, Arslanian SA: Are obesity-related metabolic risk factors modulated by the degree of insulin resistance in adolescents? Diabetes Care 2006;29:1599–1604 - PubMed
    1. Weiss R, Dufour S, Taksali SE, Tamborlane WV, Petersen KF, Bonadonna RC, Boselli L, Barbetta G, Allen K, Rife F, Savoye M, Dziura J, Sherwin R, Shulman GI, Caprio S: Prediabetes in obese youth: a syndrome of impaired glucose tolerance, severe insulin resistance, and altered myocellular and abdominal fat partitioning. Lancet 2003;362:951–957 - PMC - PubMed

Publication types