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TSC22D4 is a molecular output of hepatic wasting metabolism.

Jones A, Friedrich K, Rohm M, Schäfer M, Algire C, Kulozik P, Seibert O, Müller-Decker K, Sijmonsma T, Strzoda D, Sticht C, Gretz N, Dallinga-Thie GM, Leuchs B, Kögl M, Stremmel W, Diaz MB, Herzig S - EMBO Mol Med (2013)

Bottom Line: In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis.As a molecular cachexia output pathway, hepatic levels of the transcription factor transforming growth factor beta 1-stimulated clone (TSC) 22 D4 were increased in cancer cachexia.Therefore, hepatic TSC22D4 activity may represent a molecular rationale for peripheral energy deprivation in subjects with metabolic wasting diseases, including cancer cachexia.

View Article: PubMed Central - PubMed

Affiliation: Joint Division Molecular Metabolic Control, DKFZ-ZMBH Alliance, Network Aging Research, German Cancer Research Center (DKFZ) Heidelberg, Center for Molecular Biology (ZMBH) and University Hospital, Heidelberg University, Heidelberg, Germany.

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Serum triglycerides are lowered in cancer cachexiaBody weight development of Balb/C mice treated with PBS or 1.5 × 106 colon 26 (C26) cells over 3 weeks (means ± SEM, n ≥ 6, Two Way Repeated Measures ANOVA, Holm–Sidak post hoc).Gastrocnemius (GC) skeletal muscle weight in the same mice as in A.Abdominal and inguinal fat weight in the same mice as in A.Serum triglyceride levels in the same mice as in A. Statistical test B–D: Student's t-test.
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fig01: Serum triglycerides are lowered in cancer cachexiaBody weight development of Balb/C mice treated with PBS or 1.5 × 106 colon 26 (C26) cells over 3 weeks (means ± SEM, n ≥ 6, Two Way Repeated Measures ANOVA, Holm–Sidak post hoc).Gastrocnemius (GC) skeletal muscle weight in the same mice as in A.Abdominal and inguinal fat weight in the same mice as in A.Serum triglyceride levels in the same mice as in A. Statistical test B–D: Student's t-test.

Mentions: We employed the well-established colon (C) 26 mouse model for tumour-induced cachexia to delineate the properties of hepatic energy homeostasis during cancer cachexia (Tanaka et al, 1990). To investigate the metabolic impact of tumour growth independently of changes in food intake (anorexia), the experiment was terminated when the tumour-bearing animals had lost roughly 10% of their initial body weight (Fig 1A). At this time point, subcutaneous implantation of C26 cells into wild-type mice (Supporting Information Fig S1A) promoted loss of skeletal muscle and adipose tissue mass, while food intake as well as hepatic cholesterol and triglyceride (TG) content remained unaltered (Fig 1B and C, Supporting Information Fig S1B–D). Circulating levels of non-esterified fatty acids (NEFA) also tended to be decreased in cachectic animals (unpublished observations).


TSC22D4 is a molecular output of hepatic wasting metabolism.

Jones A, Friedrich K, Rohm M, Schäfer M, Algire C, Kulozik P, Seibert O, Müller-Decker K, Sijmonsma T, Strzoda D, Sticht C, Gretz N, Dallinga-Thie GM, Leuchs B, Kögl M, Stremmel W, Diaz MB, Herzig S - EMBO Mol Med (2013)

Serum triglycerides are lowered in cancer cachexiaBody weight development of Balb/C mice treated with PBS or 1.5 × 106 colon 26 (C26) cells over 3 weeks (means ± SEM, n ≥ 6, Two Way Repeated Measures ANOVA, Holm–Sidak post hoc).Gastrocnemius (GC) skeletal muscle weight in the same mice as in A.Abdominal and inguinal fat weight in the same mice as in A.Serum triglyceride levels in the same mice as in A. Statistical test B–D: Student's t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569644&req=5

fig01: Serum triglycerides are lowered in cancer cachexiaBody weight development of Balb/C mice treated with PBS or 1.5 × 106 colon 26 (C26) cells over 3 weeks (means ± SEM, n ≥ 6, Two Way Repeated Measures ANOVA, Holm–Sidak post hoc).Gastrocnemius (GC) skeletal muscle weight in the same mice as in A.Abdominal and inguinal fat weight in the same mice as in A.Serum triglyceride levels in the same mice as in A. Statistical test B–D: Student's t-test.
Mentions: We employed the well-established colon (C) 26 mouse model for tumour-induced cachexia to delineate the properties of hepatic energy homeostasis during cancer cachexia (Tanaka et al, 1990). To investigate the metabolic impact of tumour growth independently of changes in food intake (anorexia), the experiment was terminated when the tumour-bearing animals had lost roughly 10% of their initial body weight (Fig 1A). At this time point, subcutaneous implantation of C26 cells into wild-type mice (Supporting Information Fig S1A) promoted loss of skeletal muscle and adipose tissue mass, while food intake as well as hepatic cholesterol and triglyceride (TG) content remained unaltered (Fig 1B and C, Supporting Information Fig S1B–D). Circulating levels of non-esterified fatty acids (NEFA) also tended to be decreased in cachectic animals (unpublished observations).

Bottom Line: In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis.As a molecular cachexia output pathway, hepatic levels of the transcription factor transforming growth factor beta 1-stimulated clone (TSC) 22 D4 were increased in cancer cachexia.Therefore, hepatic TSC22D4 activity may represent a molecular rationale for peripheral energy deprivation in subjects with metabolic wasting diseases, including cancer cachexia.

View Article: PubMed Central - PubMed

Affiliation: Joint Division Molecular Metabolic Control, DKFZ-ZMBH Alliance, Network Aging Research, German Cancer Research Center (DKFZ) Heidelberg, Center for Molecular Biology (ZMBH) and University Hospital, Heidelberg University, Heidelberg, Germany.

Show MeSH
Related in: MedlinePlus