• Title/Summary/Keyword: Metabolic Hormones

Search Result 97, Processing Time 0.026 seconds

Metabolic Signaling by Adipose Tissue Hormones in Obesity (비만에서 adipose tissue 호르몬에 의한 metabolic signaling)

  • Younghoon Jang
    • Journal of Life Science
    • /
    • v.33 no.3
    • /
    • pp.287-294
    • /
    • 2023
  • Healthy adipose tissue is critical for preventing obesity by maintaining metabolic homeostasis. Adipose tissue plays an important role in energy homeostasis through glucose and lipid metabolism. Depending on nutritional status, adipose tissue expands to store lipids or can be consumed by lipolysis. The role of adipose tissue as an endocrine organ is emerging, and many studies have reported that there are various adipose tissue hormones that communicate with other organs and tissues through metabolic signaling. For example, leptin, a representative peptide hormone secreted from adipose tissues (adipokine), circulates and targets the central nervous system of the brain for appetite regression. Furthermore, adipocytes secrete inflammatory cytokines to target immune cells in adipose tissues. Not surprisingly, adipocytes can secrete fatty acid-derived hormones (lipokine) that bind to their specific receptors for paracrine and endocrine action. To understand organ crosstalk by adipose tissue hor- mones, specific metabolic signaling in adipocytes and other communicating cells should be defined. The dysfunction of metabolic signaling in adipocytes occurs in unhealthy adipose tissue in overweight and obese conditions. Therapy targeting novel adipose metabolic signaling could potentially lead to the development of an effective anti-obesity drug. This review summarizes the latest updates on adipose tissue hormone and metabolic signaling in terms of obesity and metabolic diseases.

Elevated thyroid hormones caused by high concentrate diets participate in hepatic metabolic disorders in dairy cows

  • Chen, Qu;Wu, Chen;Yao, Zhihao;Cai, Liuping;Ni, Yingdong;Mao, Shengyong
    • Animal Bioscience
    • /
    • v.35 no.8
    • /
    • pp.1184-1194
    • /
    • 2022
  • Objective: High concentrate diets are widely used to satisfy high-yielding dairy cows; however, long-term feeding of high concentrate diets can cause subacute ruminal acidosis (SARA). The endocrine disturbance is one of the important reasons for metabolic disorders caused by SARA. However, there is no current report about thyroid hormones involved in liver metabolic disorders induced by a high concentrate diet. Methods: In this study, 12 mid-lactating dairy cows were randomly assigned to HC (high concentrate) group (60% concentrate of dry matter, n = 6) and LC (low concentrate) group (40% concentrate of dry matter, n = 6). All cows were slaughtered on the 21st day, and the samples of blood and liver were collected to analyze the blood biochemistry, histological changes, thyroid hormones, and the expression of genes and proteins. Results: Compared with LC group, HC group showed decreased serum triglyceride, free fatty acid, total cholesterol, low-density lipoprotein cholesterol, increased hepatic glycogen, and glucose. For glucose metabolism, the gene and protein expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase 1 in the liver were significantly up-regulated in HC group. For lipid metabolism, the expression of sterol regulatory element-binding protein 1, long-chain acyl-CoA synthetase 1, and fatty acid synthase in the liver was decreased in HC group, whereas carnitine palmitoyltransferase 1α and peroxisome proliferator activated receptor α were increased. Serum triiodothyronine, thyroxin, free triiodothyronine (FT3), and hepatic FT3 increased in HC group, accompanied by increased expression of thyroid hormone receptor (THR) in the liver. Conclusion: Taken together, thyroid hormones may increase hepatic gluconeogenesis, β-oxidation and reduce fatty acid synthesis through the THR pathway to participate in the metabolic disorders caused by a high concentrate diet.

Studies on the Metabolic Cooperativity between Ooccte and Cumulus Cells in Mammalian Oocyte Cumulus Complexes in vitro (포유동물 난자-난구 복합체의 Metabolic cooperativity)

  • 고선근;나철호;권혁방
    • The Korean Journal of Zoology
    • /
    • v.31 no.2
    • /
    • pp.81-86
    • /
    • 1988
  • The relationship between cumulus cell expansion, cocyte maturation and metabolic cooperativitiy was investigated by using mouse and pig cocyte-cumulus complexes in vitro. Cocyte germinal vesicle breakdown (GVBD) and cumulus expansion were manipulated with hormones or reagents which increase intracellular cAMP leveL Metabolic cooperativity between oocyte and cumulus cells was assessed by determination of the fraction of radiolabelled uridine marker that was transferred from the cumulus mass to the oocyte. Uptake of uddine marker by mouse and pig cumulus mass was increased by about fourfold of basal level with the stimulation of hormones (human choriononic gonadotrophin, HCG; follicle stimulating hormone, FSH) or cyclic AMP sttmulators (3-isobutyl-1-methylxanthine, IBMX; forskolin) during culture. However, the fraction of uridine that was transferred from the cumulus mass to the cocyte (transfer ratio) was gradually decreased during culture, irrespective with the presence of hormones or stimulators. The decrease of the transfer ratio was not correlated with the state of occyte whether they have GV or not, or with the degree of cumulus expansion. In mouse complexes, HCG induced more significant reducton of transfer ratio than other treatments. These results do not support the idea that modulations of metabolic cooperativity between cumulus cells and oocytes are important for the regulation of meiotic resumption in mammals.

  • PDF

Metabolic Interactions of Cannabinoids with Steroid Hormones

  • Watanabe, Kazuhito
    • Proceedings of the Korean Society of Applied Pharmacology
    • /
    • 2007.11a
    • /
    • pp.57-64
    • /
    • 2007
  • Metabolic interactions of the three major cannabinoids, ${\Delta}^9$-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabinol (CBN) with steroid hormones were investigated. These cannabioids concentration-dependently inhibited $3{\beta}$-hydroxysteroid dehydrogenase and $17{\alpha}$-hydroxylase in rat adrenal and testis microsomes. CBD and CBN were the most potent inhibitors of $3{\beta}$-phydroxysteroid dehydrogenase and progesterone $17{\alpha}$-hydroxylase, respectively, in rat testis microsomes. Three cannabinoids highly attenuated hCG-stimulated testosterone production in rat testicular interstitial cells. These cannabinoids also decreased in levels of mRNA and protein of StAR in the rat testis cells. These results indicate that the cannabinoids could interact with steroid hormones, and exert their modulatory effects on endocrine and testicular functions. Metabolic interaction of a THC metabolite, $7{\beta}$-hydroxy-${\Delta}^8$-THC with steroids is also investigated. Monkey liver microsomes catalyzed the stereoselective oxidation of $7{\beta}$-hydroxy-${\Delta}^8$-THC to 7-oxo-${\Delta}^8$-THC, so-called microsomal alcohol oxygenase (MALCO). The reaction is catalyzed by CYP3A8 in the monkey liver microsomes, and required NADH as well as NADPH as an efficient cofactor, and its activity is stimulated by some steroids such as testosterone and progesterone. Kinetic analyses revealed that MALCO-catalyze reaction showed positive cooperativity. In order to explain the metabolic interaction between the cannabinoid metabolite and testosterone, we propose a novel kinetic model involving at least three binding sites for mechanism of the metabolic interactions.

  • PDF

Effect of zinc supplementation on insulin resistance and metabolic risk factors in obese Korean women

  • Kim, Ji-Hye;Lee, Sun-Ju
    • Nutrition Research and Practice
    • /
    • v.6 no.3
    • /
    • pp.221-225
    • /
    • 2012
  • Zinc deficiency is known to be associated with insulin resistance in obese individuals. This study was performed to evaluate the effect of zinc supplementation on insulin resistance and metabolic risk factors in obese Korean women. Forty obese women (body mass index (BMI) ${\geq}25kg/m^2$) aged 19-28 years were recruited for this study. Twenty women of the study group took 30 mg/day of supplemental zinc as zinc gluconate for 8 weeks and 20 women of control group took placebo. Usual dietary zinc intake was estimated from 3-day diet records. Insulin resistances were measured using Homeostasis model assessment (HOMA) indices, and insulin sensitivities Matsuda indices, which were calculated using oral glucose tolerance test data. Metabolic risk factors, such as waist circumference, blood pressure, fasting glucose, triglyceride, high density lipoprotein (HDL) cholesterol, and adipocyte hormones such as leptin, and adiponectin were also measured. At the beginning of study, dietary zinc averaged 7.31 mg/day and serum zinc averaged $12.98{\mu}mol/L$ in the study group. Zinc supplementation increased serum zinc by 15% and urinary zinc by 56% (P < 0.05). HOMA values tended to decrease and insulin sensitivity increased slightly in the study group, but not significantly so. BMI, waist circumference, blood pressure, blood glucose, triglyceride, HDL cholesterol, and adipocyte hormones did not change in either the study or control group. These results suggest that zinc status may not affect insulin resistance and metabolic risk factors in obese Korean women. Further research is required on a larger cohort with a longer follow-up to determine the effects of zinc status on insulin resistance and metabolic variables.

Lipid Metabolism, Disorders and Therapeutic Drugs - Review

  • Natesan, Vijayakumar;Kim, Sung-Jin
    • Biomolecules & Therapeutics
    • /
    • v.29 no.6
    • /
    • pp.596-604
    • /
    • 2021
  • Different lifestyles have an impact on useful metabolic functions, causing disorders. Different lipids are involved in the metabolic functions that play various vital roles in the body, such as structural components, storage of energy, in signaling, as biomarkers, in energy metabolism, and as hormones. Inter-related disorders are caused when these functions are affected, like diabetes, cancer, infections, and inflammatory and neurodegenerative conditions in humans. During the Covid-19 period, there has been a lot of focus on the effects of metabolic disorders all over the world. Hence, this review collectively reports on research concerning metabolic disorders, mainly cardiovascular and diabetes mellitus. In addition, drug research in lipid metabolism disorders have also been considered. This review explores lipids, metabolism, lipid metabolism disorders, and drugs used for these disorders.

Bile Acids and the Metabolic Disorders (담즙산과 대사질환)

  • Roh, Ji Hye;Yoon, Jeong-Hyun
    • Korean Journal of Clinical Pharmacy
    • /
    • v.28 no.4
    • /
    • pp.273-278
    • /
    • 2018
  • Bile acids are major constituents of bile and known to help absorb dietary fat and fat-soluble vitamins in the gastrointestinal tract. In the past few decades, many studies have shown that bile acids not only play a role in fat digestion but also function as broad range of signal transduction hormones by binding to various receptors present in cell membranes or nuclei. Bile acid receptors are distributed in a wide range of organs and tissues in the human body. They perform multitudes of physiological functions with complex mechanisms. When bile acids bind to their receptors, they regulate fat and glucose metabolism in a tissue-specific way. In addition, bile acids are shown to inhibit inflammation and fibrosis in the liver. Considering the roles of bile acids as metabolic regulators, bile acids and their receptors can be very attractive targets in treating metabolic disorders. In the future, if roles of bile acids and their receptors are further clarified, they will be the novel target of drugs in the treatment of various metabolic diseases.

A systematic review of the biological mechanisms linking physical activity and breast cancer

  • Hong, Bok Sil;Lee, Kang Pa
    • Korean Journal of Exercise Nutrition
    • /
    • v.24 no.3
    • /
    • pp.25-31
    • /
    • 2020
  • [Purpose] Epidemiological evidence has shown that leisure-time physical activity and structured exercise before and after breast cancer diagnosis contribute to reducing the risk of breast cancer recurrence and mortality. Thus, in this review, we aimed to summarize the physical activity-dependent regulation of systemic factors to understand the biological and molecular mechanisms involved in the initiation, progression, and survival of breast cancer. [Methods] We systematically reviewed the studies on 1) the relationship between physical activity and the risk of breast cancer, and 2) various systemic factors induced by physical activity and exercise that are potentially linked to breast cancer outcomes. To perform this literature review, PubMed database was searched using the terms "Physical activity OR exercise" and "breast cancer", until August 5th, 2020; then, we reviewed those articles related to biological mechanisms after examining the resulting search list. [Results] There is strong evidence that physical activity reduces the risk of breast cancer, and the protective effect of physical activity on breast cancer has been achieved by long-term regulation of various circulatory factors, such as sex hormones, metabolic hormones, inflammatory factors, adipokines, and myokines. In addition, physical activity substantially alters wholebody homeostasis by affecting numerous other factors, including plasma metabolites, reactive oxygen species, and microRNAs as well as exosomes and gut microbiota profile, and thereby every cell and organ in the whole body might be ultimately affected by the biological perturbation induced by physical activity and exercise. [Conclusion] The understanding of integrative mechanisms will enhance how physical activity can ultimately influence the risk and prognosis of various cancers, including breast cancer. Furthermore, physical activity could be considered an efficacious non-pharmacological therapy, and the promotion of physical activity is probably an effective strategy in primary cancer prevention.

Factors Associated with Weight Gain and Its Prevention Strategies (체중 증가의 관련 요인과 예방책)

  • Seung Hee Kim
    • Archives of Obesity and Metabolism
    • /
    • v.2 no.2
    • /
    • pp.37-44
    • /
    • 2023
  • Weight gain is defined as the increase in body weight, increasing the prevalence of obesity, and results in metabolic diseases. Weight gain was reportedly caused by the interaction between the obesogenic environmental factors and individual metabolic factors. Sociodemographic and environmental factors (demographic factors, lifestyle/behavioral factors, food/nutritional factors, socioeconomic factors), drug-related secondary causes (some of the corticosteroids, antihyperglycemics, antihypertensives, antidepressants, etc.), and metabolic factors (aging and hormonal changes, menopause and decreased sex hormones, decreased adipocyte degradation, decreased fibroblast growth factor 21, central sympathetic nervous system hyperactivity, decreased sympathetic-adrenomedullary system activity) are significant factors related to weight gain. It is crucial to prevent weight gain and maintain an ideal weight, but studies on the risk factors of weight gain are insufficient. Therefore, this study evaluated the factors associated with weight gain to find strategies for preventing unnecessary weight gain.

The Impairment of Thyroid Hormones Homeostasis after Short-Term Exposure to Di(2-ethylhexyl)phthalate in Adolescent Male Rats

  • Kim, Sang-Yon;Hong, Yeon-Pyo;Yang, Yun-Jung
    • Development and Reproduction
    • /
    • v.25 no.4
    • /
    • pp.293-298
    • /
    • 2021
  • Di(2-ethylhexyl)phthalate (DEHP) could induce metabolic disorders through interfering with thyroid homeostasis. Therefore, we evaluated the effects of short term to environmental relevant doses of DEHP on thyroid hormones. Four week old Sprague-Dawley (SD) rats were treated with vehicle (corn oil), and DEHP 0.75, 7.5, and 150 mg/kg/day. The rats were treated with once daily by oral gavage and were sacrificed with after 1 week. They were measured body weight and relative thyroid weight, serum thyroid hormones and histological changes of thyroid. There was no difference in body weight between the control and DEHP exposed rats. Relative thyroid weight in DEHP 150 mg/kg/day treated group was significantly lower than control. Serum thyroxine levels was decreased in rats exposed to 0.75 and 150 mg/kg/day DEHP. No histological changes were observed in the thyroid of rats administered DEHP compared to control. Exposure to DEHP at environmental relevant levels, even short-term exposure, can cause hypothyroidism in adolescent rats even the exposure period is relative short.