CD36 deficiency predisposing young children to fasting hypoglycemia

Hironori Nagasaka, Tohru Yorifuji, Tomozumi Takatani, Yoshiyuki Okano, Hirokazu Tsukahara, Hidekatsu Yanai, Ken Ichi Hirano, Shu Ping Hui, Satoshi Hirayama, Tetsuya Ito, Hitoshi Chiba, Takashi Miida

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Fatty acid (FA) β-oxidation defects cause hypoglycemia. Our aim was to determine if CD36-a membrane transporter for long-chain FAs-deficiency predisposes children to hypoglycemia. After overnight fasting, we measured parameters for carbohydrate and FA metabolisms at 12-, 14-, and 16-hour fasting points in 51 preschool children with histories of episodic hypoglycemia and 49 age-matched healthy controls. Simultaneously, the expressions of CD36 on platelets and monocytes were examined to determine the phenotypes. Six of the 51 hypoglycemic children and none of the 49 control children were diagnosed as having type I CD36 deficiency. Four and 3 children were diagnosed as having type II CD36 deficiency, respectively. Hypoglycemia was often recurrent in the type I CD36 group. At any fasting point, the type I CD36 group showed significantly lower blood glucose and insulin concentrations than the other groups: glucose, P < .001 vs control group and P < .01 or P < .001 vs type II/wild-type CD36 hypoglycemic groups; insulin, P < .001 vs control group and P < .01 vs type II/wild-type CD36 hypoglycemic groups. Free FA concentration in the type I group was always 1.5- to 2.0-fold higher than that in the other groups, whereas the total ketone body concentration was consistently about two thirds of that in the other groups. Among the type II, wild-type, and control groups, there were no significant differences in the parameters except that the wild-type group showed significantly lower FFA concentration (P < .05). These results suggested that type I CD36 deficiency but not type II CD36 deficiency predisposes preschool children to hypoglycemia.

Original languageEnglish
Pages (from-to)881-887
Number of pages7
JournalMetabolism: Clinical and Experimental
Volume60
Issue number6
DOIs
Publication statusPublished - 01-06-2011

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Hypoglycemia
Hypoglycemic Agents
Fasting
Preschool Children
Control Groups
Fatty Acids
Insulin
Ketone Bodies
Membrane Transport Proteins
Nonesterified Fatty Acids
Blood Glucose
Monocytes
Blood Platelets
Carbohydrates
Platelet Glycoprotein IV Deficiency
Phenotype
Glucose

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Nagasaka, H., Yorifuji, T., Takatani, T., Okano, Y., Tsukahara, H., Yanai, H., ... Miida, T. (2011). CD36 deficiency predisposing young children to fasting hypoglycemia. Metabolism: Clinical and Experimental, 60(6), 881-887. https://doi.org/10.1016/j.metabol.2010.08.008
Nagasaka, Hironori ; Yorifuji, Tohru ; Takatani, Tomozumi ; Okano, Yoshiyuki ; Tsukahara, Hirokazu ; Yanai, Hidekatsu ; Hirano, Ken Ichi ; Hui, Shu Ping ; Hirayama, Satoshi ; Ito, Tetsuya ; Chiba, Hitoshi ; Miida, Takashi. / CD36 deficiency predisposing young children to fasting hypoglycemia. In: Metabolism: Clinical and Experimental. 2011 ; Vol. 60, No. 6. pp. 881-887.
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Nagasaka, H, Yorifuji, T, Takatani, T, Okano, Y, Tsukahara, H, Yanai, H, Hirano, KI, Hui, SP, Hirayama, S, Ito, T, Chiba, H & Miida, T 2011, 'CD36 deficiency predisposing young children to fasting hypoglycemia', Metabolism: Clinical and Experimental, vol. 60, no. 6, pp. 881-887. https://doi.org/10.1016/j.metabol.2010.08.008

CD36 deficiency predisposing young children to fasting hypoglycemia. / Nagasaka, Hironori; Yorifuji, Tohru; Takatani, Tomozumi; Okano, Yoshiyuki; Tsukahara, Hirokazu; Yanai, Hidekatsu; Hirano, Ken Ichi; Hui, Shu Ping; Hirayama, Satoshi; Ito, Tetsuya; Chiba, Hitoshi; Miida, Takashi.

In: Metabolism: Clinical and Experimental, Vol. 60, No. 6, 01.06.2011, p. 881-887.

Research output: Contribution to journalArticle

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T1 - CD36 deficiency predisposing young children to fasting hypoglycemia

AU - Nagasaka, Hironori

AU - Yorifuji, Tohru

AU - Takatani, Tomozumi

AU - Okano, Yoshiyuki

AU - Tsukahara, Hirokazu

AU - Yanai, Hidekatsu

AU - Hirano, Ken Ichi

AU - Hui, Shu Ping

AU - Hirayama, Satoshi

AU - Ito, Tetsuya

AU - Chiba, Hitoshi

AU - Miida, Takashi

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Fatty acid (FA) β-oxidation defects cause hypoglycemia. Our aim was to determine if CD36-a membrane transporter for long-chain FAs-deficiency predisposes children to hypoglycemia. After overnight fasting, we measured parameters for carbohydrate and FA metabolisms at 12-, 14-, and 16-hour fasting points in 51 preschool children with histories of episodic hypoglycemia and 49 age-matched healthy controls. Simultaneously, the expressions of CD36 on platelets and monocytes were examined to determine the phenotypes. Six of the 51 hypoglycemic children and none of the 49 control children were diagnosed as having type I CD36 deficiency. Four and 3 children were diagnosed as having type II CD36 deficiency, respectively. Hypoglycemia was often recurrent in the type I CD36 group. At any fasting point, the type I CD36 group showed significantly lower blood glucose and insulin concentrations than the other groups: glucose, P < .001 vs control group and P < .01 or P < .001 vs type II/wild-type CD36 hypoglycemic groups; insulin, P < .001 vs control group and P < .01 vs type II/wild-type CD36 hypoglycemic groups. Free FA concentration in the type I group was always 1.5- to 2.0-fold higher than that in the other groups, whereas the total ketone body concentration was consistently about two thirds of that in the other groups. Among the type II, wild-type, and control groups, there were no significant differences in the parameters except that the wild-type group showed significantly lower FFA concentration (P < .05). These results suggested that type I CD36 deficiency but not type II CD36 deficiency predisposes preschool children to hypoglycemia.

AB - Fatty acid (FA) β-oxidation defects cause hypoglycemia. Our aim was to determine if CD36-a membrane transporter for long-chain FAs-deficiency predisposes children to hypoglycemia. After overnight fasting, we measured parameters for carbohydrate and FA metabolisms at 12-, 14-, and 16-hour fasting points in 51 preschool children with histories of episodic hypoglycemia and 49 age-matched healthy controls. Simultaneously, the expressions of CD36 on platelets and monocytes were examined to determine the phenotypes. Six of the 51 hypoglycemic children and none of the 49 control children were diagnosed as having type I CD36 deficiency. Four and 3 children were diagnosed as having type II CD36 deficiency, respectively. Hypoglycemia was often recurrent in the type I CD36 group. At any fasting point, the type I CD36 group showed significantly lower blood glucose and insulin concentrations than the other groups: glucose, P < .001 vs control group and P < .01 or P < .001 vs type II/wild-type CD36 hypoglycemic groups; insulin, P < .001 vs control group and P < .01 vs type II/wild-type CD36 hypoglycemic groups. Free FA concentration in the type I group was always 1.5- to 2.0-fold higher than that in the other groups, whereas the total ketone body concentration was consistently about two thirds of that in the other groups. Among the type II, wild-type, and control groups, there were no significant differences in the parameters except that the wild-type group showed significantly lower FFA concentration (P < .05). These results suggested that type I CD36 deficiency but not type II CD36 deficiency predisposes preschool children to hypoglycemia.

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Nagasaka H, Yorifuji T, Takatani T, Okano Y, Tsukahara H, Yanai H et al. CD36 deficiency predisposing young children to fasting hypoglycemia. Metabolism: Clinical and Experimental. 2011 Jun 1;60(6):881-887. https://doi.org/10.1016/j.metabol.2010.08.008