scholarly journals Association of the thyroid hormone responsive spot 14 alpha gene with growth-related traits in Korean native chicken

2020 ◽  
Vol 33 (11) ◽  
pp. 1755-1762
Author(s):  
Muhammad Cahyadi ◽  
Hee-Bok Park ◽  
Dong Won Seo ◽  
Shil Jin ◽  
Nuri Choi ◽  
...  

Objective: Thyroid hormone responsive spot 14 alpha (THRSP) has been used to investigate the regulation of de novo lipogenesis because the variation of THRSP mRNA content in the tissue affects directly the ability of that tissue to synthetize lipids. Also, this gene responds to thyroid hormone stimulation and high level of carbohydrate feeding or insulin-injection. This study was carried out to investigate variations within THRSP and their effects on body and carcass weights in Korean native chicken (KNC).Methods: A total of 585 chickens which represent the five lines of KNC (Black, Gray-Brown, Red-Brown, White, and Yellow-Brown) were reared and body weight data were recorded every two weeks from hatch until 20 weeks of age. Polymerase chain reaction- restriction fragment length polymorphism, DNA chips for Agilent 2100 Bioanalyzer, and Fluidigm Genotyping Technology, were applied to genotype selected markers. A linear mixed-effect model was used to access association between these single nucleotide polymorphism (SNP) markers and growth-related traits.Results: A total of 30 polymorphisms were investigated in THRSP. Of these, nine SNPs for loci were selected to perform association analyses. Significant associations were detected between g.-49G>T SNP with body weight at 20 weeks of age (BW20), g.451T>C SNP with growth at 10 to 12 weeks of age (GR10-12), and g.1432A>C SNP with growth at 14 to 16 weeks trait (GR14-16) and body weight at 18 weeks of age (BW18). Moreover, diplotype of the THRSP gene significantly affected body weight at 12 weeks of age (BW12) and GR10-12 traits. Diplotype of ht1/ht2 was favorable for BW12 and GR10-12 traits.Conclusion: These results suggest that THRSP can be regarded as a candidate gene for growth traits in KNC.

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3343-3350 ◽  
Author(s):  
Qihong Zhu ◽  
Grant W. Anderson ◽  
Gregory T. Mucha ◽  
Elizabeth J. Parks ◽  
Jennifer K. Metkowski ◽  
...  

Abstract We generated a Spot 14 null mouse to assess the role of Spot 14 in de novo lipid synthesis and report the Spot 14 null mouse exhibits a phenotype in the lactating mammary gland. Spot 14 null pups nursed by Spot 14 null dams gain significantly less weight than wild-type pups nursed by wild-type dams. In contrast, Spot 14 null pups nursed by heterozygous dams show similar weight gain to wild-type littermates. We found the triglyceride content in Spot 14 null milk is significantly reduced. We demonstrate this reduction is the direct result of decreased de novo lipid synthesis in lactating mammary glands, corroborated by a marked reduction of medium-chain fatty acids in the triglyceride pool. Importantly, the reduced lipogenic rate is not associated with significant changes in the activities or mRNA of key lipogenic enzymes. Finally, we report the expression of a Spot 14-related gene in liver and adipose tissue, which is absent in the lactating mammary gland. We suggest that expression of both the Spot 14 and Spot 14-related proteins is required for maximum efficiency of de novo lipid synthesis in vivo and that these proteins impart a novel mechanism regulating de novo lipogenesis.


2018 ◽  
Vol 31 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Prabuddha Manjula ◽  
Hee-Bok Park ◽  
Dongwon Seo ◽  
Nuri Choi ◽  
Shil Jin ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A19-A20
Author(s):  
Emmanuel Quaye ◽  
Andrew Grover ◽  
Robert Brychta ◽  
John Christensen ◽  
Megan S Startzell ◽  
...  

Abstract Leptin is an adipokine that signals energy sufficiency. In rodents, leptin deficiency is associated with decreased body temperature and energy expenditure (EE), which is reversed with leptin replacement. Leptin’s role in EE in humans is unclear; however, one study of 10% weight-reduced healthy subjects suggested that leptin replacement to pre-weight loss levels restored the decline in EE, thyroid hormone, and catecholamines associated with weight loss. Patients with lipodystrophy (LD) are characterized by deficiency of adipose tissue and can serve as models to study effects of leptin deficiency and replacement in humans. We hypothesized that treatment with recombinant leptin (metreleptin) in patients with LD would increase EE, thyroid hormone, and catecholamines. We conducted a non-randomized crossover study of 25 patients with LD who were hospitalized for 19 days on an iso-caloric diet. The initiation cohort consisted of 17 patients with no prior exposure to metreleptin, who were first studied for 5 days without metreleptin (period 1), then were treated with metreleptin for 14 days (period 2). The withdrawal cohort consisted of 8 previously metreleptin-treated patients who were continued on metreleptin for the first 5 days of the study (period 1), then were taken off metreleptin for 14 days (period 2). At the end of each period, we measured 24-hour EE (TEE) and resting EE (REE) using indirect calorimetry and free T3, T4, epinephrine, norepinephrine and dopamine after an 8–12 hour fast. In the leptin initiation cohort, TEE and REE decreased from 2402±383 kcal/day and 1805±332 kcal/day to 2272±396 kcal/day (p=0.003) and 1688±318 kcal/day (p=0.03), respectively. Free T3 increased from median (IQR) 248 (200, 270) pg/mL to 295 (259, 315) (p=0.006). No changes in catecholamines were observed in the initiation cohort. In the withdrawal cohort, free T3 decreased from 295 (267, 331) pg/mL to 265 (237, 323) (p=0.008), free T4 decreased from 1.2 ±0.2 ng/dL to 1.0±0.2 (p=0.002), and norepinephrine decreased from 191±70 pg/mL to 112±47 (p=0.03) after metreleptin withdrawal. No changes in EE, epinephrine or dopamine were observed in the withdrawal cohort. Contrary to previous studies in rodents and healthy humans, we found that introduction of metreleptin reduced EE in patients with LD. Consistent with rodent and prior human data, patients with LD had increased thyroid hormone on metreleptin, which would be expected to increase EE. The discrepancy in EE compared to other models may be due to metreleptin-induced correction of severe metabolic derangements in LD, including reduction in energy-requiring processes such as de novo lipogenesis and gluconeogenesis. These changes may offset increases in leptin-induced mediators of increased EE, such as thyroid hormone.


2006 ◽  
Vol 291 (1) ◽  
pp. E23-E37 ◽  
Author(s):  
Kevin D. Hall

Changes in body weight and composition are the result of complex interactions among metabolic fluxes contributing to macronutrient balances. To better understand these interactions, a mathematical model was constructed that used the measured dietary macronutrient intake during semistarvation and refeeding as model inputs and computed whole body energy expenditure, de novo lipogenesis, and gluconeogenesis as well as turnover and oxidation of carbohydrate, fat, and protein. Published in vivo human data provided the basis for the model components that were integrated by fitting a few unknown parameters to the classic Minnesota human starvation experiment. The model simulated the measured body weight and fat mass changes during semistarvation and refeeding and predicted the unmeasured metabolic fluxes underlying the body composition changes. The resting metabolic rate matched the experimental measurements and required a model of adaptive thermogenesis. Refeeding caused an elevation of de novo lipogenesis that, along with increased fat intake, resulted in a rapid repletion and overshoot of body fat. By continuing the computer simulation with the prestarvation diet and physical activity, the original body weight and composition were eventually restored, but body fat mass was predicted to take more than one additional year to return to within 5% of its original value. The model was validated by simulating a recently published short-term caloric restriction experiment without changing the model parameters. The predicted changes in body weight, fat mass, resting metabolic rate, and nitrogen balance matched the experimental measurements, thereby providing support for the validity of the model.


2013 ◽  
Vol 40 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Muhammad Cahyadi ◽  
Dongwon Seo ◽  
Shil Jin ◽  
Nuri Choi ◽  
Hee-Bok Park ◽  
...  

2012 ◽  
Vol 303 (5) ◽  
pp. E624-E634 ◽  
Author(s):  
Vidya Vaidyanathan ◽  
Raul A. Bastarrachea ◽  
Paul B. Higgins ◽  
V. Saroja Voruganti ◽  
Subhash Kamath ◽  
...  

The goal of this study was to determine whether administration of the CB1 cannabinoid receptor antagonist rimonabant would alter fatty acid flux in nonhuman primates. Five adult baboons ( Papio Sp) aged 12.1 ± 4.7 yr (body weight: 31.9 ± 2.1 kg) underwent repeated metabolic tests to determine fatty acid and TG flux before and after 7 wk of treatment with rimonabant (15 mg/day). Animals were fed ad libitum diets, and stable isotopes were administered via diet (d31-tripalmitin) and intravenously (13C4-palmitate, 13C1-acetate). Plasma was collected in the fed and fasted states, and blood lipids were analyzed by GC-MS. DEXA was used to assess body composition and a hyperinsulinemic euglycemic clamp used to assess insulin-mediated glucose disposal. During the study, no changes were observed in food intake, body weight, plasma, and tissue endocannabinoid concentrations or the quantity of liver-TG fatty acids originating from de novo lipogenesis (19 ± 6 vs. 16 ± 5%, for pre- and posttreatment, respectively, P = 0.39). However, waist circumference was significantly reduced 4% in the treated animals ( P < 0.04), glucose disposal increased 30% ( P = 0.03), and FFA turnover increased 37% ( P = 0.02). The faster FFA flux was consistent with a 43% reduction in these fatty acids used for TRL-TG synthesis (40 ± 3 vs. 23 ± 4%, P = 0.02) and a twofold increase in TRL-TG turnover (1.5 ± 0.9 vs. 3.1 ± 1.4 μmol·kg−1·h−1, P = 0.03). These data support the potential for a strong effect of CB1 receptor antagonism at the level of adipose tissue, resulting in improvements in fasting turnover of fatty acids at the whole body level, central adipose storage, and significant improvements in glucose homeostasis.


Endocrinology ◽  
2001 ◽  
Vol 142 (10) ◽  
pp. 4363-4370 ◽  
Author(s):  
Qihong Zhu ◽  
Ami Mariash ◽  
Mark R. Margosian ◽  
Sunil Gopinath ◽  
Mohammod T. Fareed ◽  
...  

2014 ◽  
Vol 52 (08) ◽  
Author(s):  
T Tolstik ◽  
C Marquardt ◽  
C Matthäus ◽  
C Beleites ◽  
C Krafft ◽  
...  

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