Preliminary Investigation of Bottlenose Dolphins (<i>Tursiops truncatus</i>) for<i>hfe</i>Gene–related Hemochromatosis

Phillips, Brianne E.; Venn‐Watson, Stephanie; Archer, Linda L.; Nollens, Hendrik H.; Wellehan, James F. X.

doi:10.7589/2013-08-212

Cited by 6 publications

(3 citation statements)

References 16 publications

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“…p.S88T occurs in a highly conserved region involved in the interaction of HFE and TFRC [244]. Bottle-nosed dolphins ( Tursiops truncatus ) also develop iron overload [245,246] but sequencing dolphin hfe did not reveal deleterious mutations [247]. Red deer with iron storage disease ( Cervus elaphus elaphus ) did not have pathogenic HFE mutations [248].…”

Section: Hfe Mutations and Iron Overload In Other Mammalsmentioning

confidence: 99%

HFE gene: Structure, function, mutations, and associated iron abnormalities

Barton

Edwards

Acton

2015

Gene

111

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The hemochromatosis gene HFE was discovered in 1996, more than a century after clinical and pathologic manifestations of hemochromatosis were reported. Linked to the major histocompatibility complex (MHC) on chromosome 6p, HFE encodes the MHC class I-like protein HFE that binds beta-2 microglobulin. HFE influences iron absorption by modulating the expression of hepcidin, the main controller of iron metabolism. Common HFE mutations account for ~90% of hemochromatosis phenotypes in whites of western European descent. We review HFE mapping and cloning, structure, promoters and controllers, and coding region mutations, HFE protein structure, cell and tissue expression and function, mouse Hfe knockouts and knockins, and HFE mutations in other mammals with iron overload. We describe the pertinence of HFE and HFE to mechanisms of iron homeostasis, the origin and fixation of HFE polymorphisms in European and other populations, and the genetic and biochemical basis of HFE hemochromatosis and iron overload.

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Section: Hfe Mutations and Iron Overload In Other Mammalsmentioning

confidence: 99%

HFE gene: Structure, function, mutations, and associated iron abnormalities

Barton

Edwards

Acton

2015

Gene

111

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“…High ferritin and iron in dolphins, which includes excessive iron deposition primarily in the liver’s Kupffer cells, is progressive with age and associated with elevated insulin, lipids, and liver enzymes [ 10 , 11 , 21 , 22 ]. This metabolic state in dolphins is associated with neither mutations in the HFE gene nor increases in acute phase proteins [ 23 , 24 ]. The underlying cause of high ferritin in dolphins remain unknown.…”

Section: Introductionmentioning

confidence: 99%

Increased Dietary Intake of Saturated Fatty Acid Heptadecanoic Acid (C17:0) Associated with Decreasing Ferritin and Alleviated Metabolic Syndrome in Dolphins

et al. 2015

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Similar to humans, bottlenose dolphins (Tursiops truncatus) can develop metabolic syndrome and associated high ferritin. While fish and fish-based fatty acids may protect against metabolic syndrome in humans, findings have been inconsistent. To assess potential protective factors against metabolic syndrome related to fish diets, fatty acids were compared between two dolphin populations with higher (n = 30, Group A) and lower (n = 19, Group B) mean insulin (11 ± 12 and 2 ± 5 μIU/ml, respectively; P < 0.0001) and their dietary fish. In addition to higher insulin, triglycerides, and ferritin, Group A had lower percent serum heptadecanoic acid (C17:0) compared to Group B (0.3 ± 0.1 and 1.3 ± 0.4%, respectively; P < 0.0001). Using multivariate stepwise regression, higher percent serum C17:0, a saturated fat found in dairy fat, rye, and some fish, was an independent predictor of lower insulin in dolphins. Capelin, a common dietary fish for Group A, had no detectable C17:0, while pinfish and mullet, common in Group B’s diet, had C17:0 (41 and 67 mg/100g, respectively). When a modified diet adding 25% pinfish and/or mullet was fed to six Group A dolphins over 24 weeks (increasing the average daily dietary C17:0 intake from 400 to 1700 mg), C17:0 serum levels increased, high ferritin decreased, and blood-based metabolic syndrome indices normalized toward reference levels. These effects were not found in four reference dolphins. Further, higher total serum C17:0 was an independent and linear predictor of lower ferritin in dolphins in Group B dolphins. Among off the shelf dairy products tested, butter had the highest C17:0 (423mg/100g); nonfat dairy products had no detectable C17:0. We hypothesize that humans’ movement away from diets with potentially beneficial saturated fatty acid C17:0, including whole fat dairy products, could be a contributor to widespread low C17:0 levels, higher ferritin, and metabolic syndrome.

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“…Hemosiderosis is excessive iron deposition in tissues without pathologic sequelae. 1,6 Hemochromatosis, also known as iron storage disease (ISD), is well-documented in a number of animal species, 2,4,7,8,[10][11][12][13] including various species of wild and captive birds. 16 Fruit or nectar-eating avian species such as birds of paradise, toucans, mynahs, starlings, lorikeets, and rarely other psittacines may be particularly prone to developing ISD.…”

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confidence: 99%

Hepatic lesions associated with iron accumulation in captive kori bustards (Ardeotis kori)

Cudd¹,

Garner²,

Cartoceti

et al. 2021

Vet Pathol

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There are anecdotal reports of iron storage disease in captive kori bustards ( Ardeotis kori), but detailed descriptions of this disease have not been reported. The goals of this retrospective, multi-institutional study were to (1) describe microscopic findings associated with iron accumulation in postmortem tissues of kori bustards and (2) use an adapted grading scale to score iron accumulation and associated hepatic lesions. Tissue sections from 19 adult captive kori bustards (age range 3–28 years; 12 males and 7 females) were evaluated histologically with hematoxylin and eosin, Masson’s trichrome, and Prussian blue stains, and scored for iron accumulation. Hemochromatosis was diagnosed in cases with iron storage (in hepatocytes and/or Kupffer cells) and concurrent parenchymal damage (defined as having both necrosis and fibrosis). Hemosiderosis was diagnosed in animals with evidence of iron storage without necrosis or fibrosis. Ten of the 19 cases (age range 8–27 years; 7 males and 3 females) were diagnosed with hemochromatosis, including 6 with mild disease, 3 with moderate disease, and 1 with severe disease. Histologic evidence of iron accumulation was also identified in kidney, intestinal tract, adrenal gland, and spleen, but there were no associations between severity of iron accumulation in the liver and accumulation in other organs.

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Preliminary Investigation of Bottlenose Dolphins (Tursiops truncatus) forhfeGene–related Hemochromatosis

Cited by 6 publications

References 16 publications

HFE gene: Structure, function, mutations, and associated iron abnormalities

HFE gene: Structure, function, mutations, and associated iron abnormalities

Increased Dietary Intake of Saturated Fatty Acid Heptadecanoic Acid (C17:0) Associated with Decreasing Ferritin and Alleviated Metabolic Syndrome in Dolphins

Hepatic lesions associated with iron accumulation in captive kori bustards (Ardeotis kori)

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