scholarly journals Lactate and the GPR81 receptor in metabolic regulation: implications for adipose tissue function and fatty acid utilisation by muscle during exercise

2011 ◽  
Vol 106 (9) ◽  
pp. 1310-1316 ◽  
Author(s):  
Kieron Rooney ◽  
Paul Trayhurn
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Metabolic Regulation ◽  
Anaerobic Metabolism ◽  
Lactate Production ◽  
Muscle Lactate ◽  
Lipolytic Action ◽  
Adipose Tissue Depots ◽  
Fatty Acid Utilisation ◽  
G Protein Coupled

Lactate is increasingly recognised to be more than a simple end product of anaerobic glycolysis. Skeletal muscle and white adipose tissue are considered to be the main sites of lactate production and release. Recent studies have demonstrated that there is a specific G-protein coupled receptor for lactate, GPR81, which is expressed primarily in adipose tissue, and also in muscle. Lactate inhibits lipolysis in adipose tissue by mediating, through GPR81, the anti-lipolytic action of insulin. A high proportion (50 % or more) of the glucose utilised by white adipose tissue is converted to lactate and lactate production by the tissue increases markedly in obesity; this is likely to reflect a switch towards anaerobic metabolism with the development of hypoxia in the tissue. During exercise, there is a shift in fuel utilisation by muscle from lipid to carbohydrate, but this does not appear to be a result of the inhibition of lipolysis in the main adipose tissue depots by muscle-derived lactate. It is suggested instead that a putative autocrine lactate loop in myocytes may regulate fuel utilisation by muscle during exercise, operating via a muscle GPR81 receptor. In addition to being an important substrate, lactate is a key signal in metabolic regulation.

Sympathetic Innervation of White Adipose Tissue: to Beige or Not to Beige?

Physiology ◽  
2021 ◽  
Vol 36 (4) ◽  
pp. 246-255
Author(s):  
Heike Münzberg ◽  
Elizabeth Floyd ◽  
Ji Suk Chang
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Metabolic Regulation ◽  
Current Knowledge ◽  
Sympathetic Innervation ◽  
Neuronal Circuits ◽  
Brown Adipocytes ◽  
White Adipocyte ◽  
Obesity Research ◽  
Neuronal Regulation

Obesity research progresses in understanding neuronal circuits and adipocyte biology to regulate metabolism. However, the interface of neuro-adipocyte interaction is less studied. We summarize the current knowledge of adipose tissue innervation and interaction with adipocytes and emphasize adipocyte transitions from white to brown adipocytes and vice versa. We further highlight emerging concepts for the differential neuronal regulation of brown/beige versus white adipocyte and the interdependence of both for metabolic regulation.

White Adipose Tissue Depots in GHR−/− Mice: Age-Related Changes in Comparison to Wild-Type Controls

2011 ◽  
pp. P2-351-P2-351
Author(s):  
Lucila Sackmann Sala ◽  
Clare B Vesel ◽  
Ellen R Lubbers ◽  
Rachel D Munn ◽  
Katie M Troike ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Wild Type ◽  
Adipose Tissue Depots ◽  
Age Related ◽  
Age Related Changes

Improved metabolic regulation is associated with retinoblastoma protein gene haploinsufficiency in mice

2015 ◽  
Vol 308 (2) ◽  
pp. E172-E183 ◽  
Author(s):  
Petar D. Petrov ◽  
Joan Ribot ◽  
Andreu Palou ◽  
M. Luisa Bonet
Keyword(s):  
Adipose Tissue ◽  
Body Fat ◽  
White Adipose Tissue ◽  
Metabolic Regulation ◽  
Retinoblastoma Protein ◽  
Acid Oxidation ◽  
Mature Adult ◽  
Adult Age ◽  
Enhanced Sensitivity ◽  
Partial Deficiency

Retinoblastoma protein (pRb) is involved in the control of energy metabolism, and its inactivation protects mice against high-fat diet-induced diabesity. Here, we tested the hypothesis that partial deficiency in the Rb gene could confer metabolic advantages in front of acute challenges to metabolism and as mice age on a regular diet. Rb haploinsufficient (Rb+/−) mice and wild-type (WT) littermates were studied from weaning and characterized at 1.5–2.5 mo of age (young adults) and 6–7.5 mo of age (mature adults). Whereas no differences in body weight or composition were observed at young age, mature adult Rb+/− mice were leaner than WT littermates, displaying 36% reduced body fat content. At both ages studied, Rb+/− mice displayed improved blood lipids, enhanced sensitivity to the blood glucose-lowering effect of insulin and to the anorectic effect of leptin, and a reduced respiratory exchange ratio, indicative of an increased use of fatty acids as a fuel. Insulin sensitivity and oral fat tolerance were better maintained with age in the Rb+/− than the WT mice. Mature adult Rb+/− mice displayed gene expression changes consistent with increased fatty acid oxidation in white adipose tissue and skeletal muscle and paramount signs of browning in the inguinal white adipose tissue. In conclusion, Rb haploinsufficiency provides metabolic advantages in front of acute metabolic stressors and ameliorates body fat gain and metabolic impairments that normally accompany transition from young to mature adult age.

scholarly journals Adipose Tissue Depots and Their Cross‐Sectional Associations With Circulating Biomarkers of Metabolic Regulation

2016 ◽  
Vol 5 (5) ◽  
Author(s):  
Jane J. Lee ◽  
Kathryn A. Britton ◽  
Alison Pedley ◽  
Joseph M. Massaro ◽  
Elizabeth K. Speliotes ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Metabolic Regulation ◽  
Circulating Biomarkers ◽  
Cross Sectional ◽  
Adipose Tissue Depots

scholarly journals Differences among white adipose tissue depots in mice

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Lucila Sackmann Sala ◽  
Rachel Munn ◽  
Ellen Lubbers ◽  
Darlene E Berryman ◽  
John J Kopchick
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Adipose Tissue Depots

scholarly journals Deciphering White Adipose Tissue Heterogeneity

Biology ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 23 ◽  
Author(s):  
Quyen Luong ◽  
Jun Huang ◽  
Kevin Y. Lee
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Lineage Tracing ◽  
The Body ◽  
Functional Heterogeneity ◽  
Tissue Heterogeneity ◽  
Adipose Tissue Depots ◽  
White Adipocytes ◽  
Increased Risk ◽  
Beige Adipocytes

Adipose tissue not only stores energy, but also controls metabolism through secretion of hormones, cytokines, proteins, and microRNAs that affect the function of cells and tissues throughout the body. Adipose tissue is organized into discrete depots throughout the body, and these depots are differentially associated with insulin resistance and increased risk of metabolic disease. In addition to energy-dissipating brown and beige adipocytes, recent lineage tracing studies have demonstrated that individual adipose depots are composed of white adipocytes that are derived from distinct precursor populations, giving rise to distinct subpopulations of energy-storing white adipocytes. In this review, we discuss this developmental and functional heterogeneity of white adipocytes both between and within adipose depots. In particular, we will highlight findings from our recent manuscript in which we find and characterize three major subtypes of white adipocytes. We will discuss these data relating to the differences between subcutaneous and visceral white adipose tissue and in relationship to previous work deciphering adipocyte heterogeneity within adipose tissue depots. Finally, we will discuss the possible implications of adipocyte heterogeneity may have for the understanding of lipodystrophies.

scholarly journals Regulation of fructose 2,6-bisphosphate concentration in white adipose tissue

1985 ◽  
Vol 225 (2) ◽  
pp. 421-428 ◽  
Author(s):  
M H Rider ◽  
L Hue
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Insulin Treatment ◽  
Lactate Production ◽  
Diabetic Rats ◽  
Epididymal Fat ◽  
Lactate Output ◽  
Concentration Changes ◽  
Dose Dependent ◽  
Fat Pads

Injection of insulin to fed rats diminished the concentration of fructose 2,6-bisphosphate in white adipose tissue. Incubation of epididymal fat-pads or adipocytes with insulin stimulated lactate release and sugar detritiation and also decreased fructose 2,6-bisphosphate concentration. Such a decrease was, however, not observed in fat-pads from starved or alloxan-diabetic rats. Incubation of adipocytes from fed rats with various concentrations of glucose or fructose led to a dose-dependent rise in fructose 2,6-bisphosphate which correlated with lactate output and detritiation of 3-3H-labelled sugar. In adipocytes from fed rats, palmitate stimulated the detritiation of [3-3H]glucose without affecting lactate production and fructose 2,6-bisphosphate concentration. Incubation of epididymal fat-pads from fed rats in the presence of antimycin stimulated lactate output but decreased fructose 2,6-bisphosphate concentration. Changes in lipolytic rates brought about by noradrenaline, insulin, adenosine and corticotropin in adipocytes from fed rats were not related to changes in fructose 2,6-bisphosphate or to rates of lactate output. In fed rats, the activity of 6-phosphofructo-2-kinase was not changed after treatment of adipocytes with insulin, noradrenaline or adenosine. It is suggested that the decrease in fructose 2,6-bisphosphate concentration observed after insulin treatment can be explained by the increase in sn-glycerol 3-phosphate, an inhibitor of 6-phosphofructo-2-kinase.

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