Adipocyte differentiation of 3T3-L1 cells in serum-free hormone-supplemented media: Effects of insulin and dihydroteleocidin B.

Gamou, Shinobu; Shimizu, Nobuyoshi

doi:10.1247/csf.11.21

Cited by 11 publications

(9 citation statements)

References 18 publications

(19 reference statements)

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“…Insulin is also well-known to be a potent stimulator of adipogenesis in vitro (23,24). To the best of our knowledge, we here show for the first time that insulin treatment of diabetic animals can increase adipogenesis in situ.…”

Section: Discussionsupporting

confidence: 55%

Treatment of Diabetic Rats With Insulin or a Synthetic Insulin Receptor Agonist Peptide Leads to Divergent Metabolic Responses

et al. 2014

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In addition to lowering of blood glucose, treatment with insulin also induces lipid synthesis and storage. Patients with type 2 diabetes often suffer from lipid-related comorbidities including dyslipidemia, obesity, and fatty liver disease. We examined here in two separate studies changes in lipid dynamics in Zucker diabetic fatty (ZDF) rats, in response to 7 days of treatment with either insulin or the insulin receptor agonist peptide S597. In concert with blood glucose normalization, the treated rats displayed large increases in hepatic de novo lipid synthesis and deposition of newly synthesized lipids in adipose tissue depots, accompanied by weight gain and expansion of adipose depots. In both treatment groups, heavy water labeling revealed that after 2 h (study A), de novo lipogenesis was responsible for 80% of newly stored hepatic triglyceride (TG)-palmitate, and after 5 days (study B), ∼60% of newly deposited TG-palmitate in adipose tissues originated from this pathway. Interestingly, in both studies, treatment with the insulin mimetic peptide resulted in significantly lower blood TG levels, plasma TG production rates, and hepatic de novo synthesized fatty acid in plasma TG compared with insulin. There were no differences in plasma TG turnover (clearance rate) in response to either treatment, consistent with differential actions on the liver. These results show that in ZDF rats, treatment with a synthetic insulinreceptor-activating peptide or with insulin to lower blood glucose is accompanied by different effects on hepatic lipid anabolism and blood TG profiles.A major target of interest when treating diabetic patients with insulin is lowering of blood glucose levels through activation of distinct signaling pathways downstream of the insulin receptor (1,2) in tissues, including muscle and adipose (1,2). Insulin-regulated metabolic signaling also results in alterations of lipid homeostasis. Expansion of adipose depots is known to occur in animals as well as in diabetic patients during insulin treatment (3,4). In insulinresistant animals, there is evidence that the hepatic insulin receptor signaling pathways show differential responsiveness, such that the glucose-related pathways are more resistant than the ones orchestrating lipid responses (5). This results in the so-called insulin resistance triad, where two of the elements (hyperglycemia and hyperinsulinemia) reflect the reduced responsiveness to insulin on glucose metabolism, whereas the third element (hypertriglyceridemia) is believed to arise from the lipid-related pathways being less resistant and therefore excessively stimulated by the hyperinsulinemia (5). The hepatic metabolic response to insulin includes several processes: inhibition of endogenous glucose production (6), augmented glucose uptake (7), stimulation of de novo lipogenesis (DNL) (8), and inhibition of VLDL export

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Section: Discussionsupporting

confidence: 55%

Treatment of Diabetic Rats With Insulin or a Synthetic Insulin Receptor Agonist Peptide Leads to Divergent Metabolic Responses

et al. 2014

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“…When Balbic3T3 T mouse preadipocytes were shifted to heparinized medium containing human plasma, Scott et al (1982) demonstrated the existence of two temporal states for coupling of growth arrest and differentiation (G and 6 ). More recently, Gamou and Shimizu (1985) developed serum-free, hormone-supplemented conditions under which the stage of cell commitment to adipocyte differentiation (G,) could be separated from the stage of expression of the adipocyte phenotype (Gd). However for these latter conditions, this conclusion does not appear clearly convincing because their methodology involves the presence of a high concentration of fetal calf serum during the phase of expression of adipocyte phenotype.…”

Section: Discussionmentioning

confidence: 99%

Control of the adipogenic differentiation of 3T3‐F442A cells by retinoic acid, dexamethasone, and insulin: A topographic analysis

Pairault

Lasnier

1987

Journal Cellular Physiology

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Differentiation of 3T3-F442A adipocytes, monitored by accumulation of neutral lipid and by using the sensitive marker glycerophosphate dehydrogenase, is inhibited by incubation of confluent 3T3-F442A fibroblasts in medium containing retinoic acid or dexamethasone. When added together, dexamethasone (0.25 microM) potentiates about 50-fold the inhibitory effect of retinoic acid (10 microM). Insulin cannot counteract the retinoic acid blockade; however, it can overcome the inhibition of differentiation elicited by dexamethasone. These differential effects of insulin are used for characterizing the adipose conversion cycle. We describe cell culture conditions where terminal differentiation of 3T3-F442A preadipocytes is achieved by low, physiological levels of insulin. They include the switch from a high-serum medium containing isobutyl methyl xanthine and dexamethasone to a serum-free, hormone-supplemented medium. The data reported establish the existence of two successive states for commitment to adipogenic differentiation: a first commitment point (CA) to differentiation which requires serum adipogenic factors, and a second commitment point (CH) controlled by lipogenic hormones, namely insulin, after which terminal maturation can resume. We demonstrate that retinoic acid can prevent and interrupt differentiation by blocking the cells within the early differentiation phase.

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“…To undergo adipose differentiation, confluent 3T3-F442A cells require approximately 48 h in a medium supplemented with fetal bovine serum (FBS), which typically has high adipogenic activity6, whereas 3T3-L1 cells additionally require methyl isobutyl xanthine (MIX) and dexamethasone (Dex) in FBS medium78. If 3T3-F442A cells are cultured in the absence of fetal bovine serum or growth hormone (non-adipogenic media), the cells do not undergo adipose differentiation6.…”

mentioning

confidence: 99%

Glucocorticoid Paradoxically Recruits Adipose Progenitors and Impairs Lipid Homeostasis and Glucose Transport in Mature Adipocytes

Ayala-Sumuano

Velez-delValle

Beltrán-Langarica

et al. 2013

Sci Rep

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Chronic treatment with glucocorticoids increases the mass of adipose tissue and promotes metabolic syndrome. However little is known about the molecular effects of dexamethasone on adipose biology. Here, we demonstrated that dexamethasone induces progenitor cells to undergo adipogenesis. In the adipogenic pathway, at least two cell types are found: cells with the susceptibility to undergo staurosporine-induced adipose conversion and cells that require both staurosporine and dexamethasone to undergo adipogenesis. Dexamethasone increased and accelerated the expression of main adipogenic genes such as pparg2, cebpa and srebf1c. Also, dexamethasone altered the phosphorylation pattern of C/EBPβ, which is an important transcription factor during adipogenesis. Dexamethasone also had effect on mature adipocytes mature adipocytes causing the downregulation of some lipogenic genes, promoted a lipolysis state, and decreased the uptake of glucose. These paradoxical effects appear to explain the complexity of the action of glucocorticoids, which involves the hyperplasia of adipose cells and insulin resistance.

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Adipocyte differentiation of 3T3-L1 cells in serum-free hormone-supplemented media: Effects of insulin and dihydroteleocidin B.

Cited by 11 publications

References 18 publications

Treatment of Diabetic Rats With Insulin or a Synthetic Insulin Receptor Agonist Peptide Leads to Divergent Metabolic Responses

Treatment of Diabetic Rats With Insulin or a Synthetic Insulin Receptor Agonist Peptide Leads to Divergent Metabolic Responses

Control of the adipogenic differentiation of 3T3‐F442A cells by retinoic acid, dexamethasone, and insulin: A topographic analysis

Glucocorticoid Paradoxically Recruits Adipose Progenitors and Impairs Lipid Homeostasis and Glucose Transport in Mature Adipocytes

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