The adipocyte life cycle hypothesis

2005 ◽  
Vol 110 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Jessica Smith ◽  
Maha Al-Amri ◽  
Prabhakaran Dorairaj ◽  
Allan Sniderman
Keyword(s):  
Adipose Tissue ◽  
Life Cycle ◽  
Fatty Acid ◽  
East Asia ◽  
South East Asia ◽  
Adipocyte Size ◽  
Triacylglycerol Synthesis ◽  
Life Cycle Hypothesis ◽  
Metabolic Properties ◽  
Consequences Of Obesity

The adipocyte life cycle hypothesis states that the metabolic properties of an adipocyte vary predictably during its life cycle: that as an adipocyte matures, it accumulates triacylglycerol (triglyceride) and becomes larger; that the rates of triacylglycerol synthesis and lipolysis are matched within adipocytes and that larger adipocytes, in general, have greater rates of triacylglycerol synthesis and, concurrently, greater rates of lipolysis and, therefore, larger adipocytes have greater rates of transmembrane fatty acid flux; and that the secretion of cytokines can also be related to adipocyte size with larger adipocytes having a more unfavourable profile of cytokine secretion than smaller adipocytes. Adipocyte location is an important modifier of this relationship and the favoured sites of adipocyte proliferation are a function of gender and the position within the life cycle of the organism at which proliferation occurs. The adipocyte life cycle hypothesis posits that the metabolic consequences of obesity depend on whether expansion of adipose tissue is achieved primarily by an increase in adipocyte number or adipocyte size. This hypothesis may explain a variety of previously unanswered clinical puzzles such as the vulnerability of many peoples from South East Asia to the adverse metabolic consequences of obesity.

Lipogenic activity in Rasa Aragonesa ewes of different body condition score

2005 ◽  
Vol 85 (1) ◽  
pp. 101-105 ◽  
Author(s):  
A. Arana ◽  
J. A. Mendizabal ◽  
R. Delfa ◽  
P. Eguinoa ◽  
B. Soret ◽  
...  
Keyword(s):  
Enzyme Activity ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Body Condition ◽  
Fatty Acid Synthase ◽  
Body Condition Score ◽  
Lipogenic Enzyme ◽  
Adipocyte Size ◽  
Metabolic Characteristics ◽  
Condition Score

The aim of the study was to assess the effect of body condition score on tissue and metabolic characteristics of the adipose depots in sheep of Rasa Aragonesa breed. Ewes were uniformly assigned according to their body condition score (BCS) (scale 0 to 5), to four groups: 0.75–1.75, 2–2.75, 3–3.75, and 4–4.5. The amount of fat and the adipocyte size in the different adipose depots increased as BCS did (P < 0.001) while the number of adipocytes did not change. The greatest ability to accumulate or mobilize fat was the subcutaneous depot (slope of the regression between amount of fat and BCS, b = 1.92; P < 0.001). Fatty acid synthase (FAS) lipogenic enzyme activity was affected by BCS, while G3-PDH and G6-PDH activities were not. Key words: Adipose tissue, body condition score, adipocyte size, lipogenic enzyme activity, ewes

Why are saving rates in East Asia so high? Reviving the life cycle hypothesis

2003 ◽  
Vol 28 (2) ◽  
pp. 275-289 ◽  
Author(s):  
F. Gerard Adams ◽  
Peter A. Prazmowski
Keyword(s):  
Life Cycle ◽  
East Asia ◽  
Saving Rates ◽  
Life Cycle Hypothesis

scholarly journals Sex and depot differences in ex vivo adipose tissue fatty acid storage and glycerol-3-phosphate acyltransferase activity

2015 ◽  
Vol 308 (9) ◽  
pp. E830-E846 ◽  
Author(s):  
Maria Morgan-Bathke ◽  
Liang Chen ◽  
Elisabeth Oberschneider ◽  
Debra Harteneck ◽  
Michael D. Jensen
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Ex Vivo ◽  
Human Adipose Tissue ◽  
Adipocyte Size ◽  
Enzyme Activity Assay ◽  
Acyltransferase Activity ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid ◽  
Relative Contribution

Adipose tissue fatty acid storage varies according to sex, adipose tissue depot, and degree of fat gain. However, the mechanism(s) for these variations is not completely understood. We examined whether differences in adipose tissue glycerol-3-phosphate acyltransferase (GPAT) might play a role in these variations. We optimized an enzyme activity assay for total GPAT and GPAT1 activity in human adipose tissue and measured GPAT activity. Omental and subcutaneous adipose tissue was collected from obese and nonobese adults for measures of GPAT and GPAT1 activities, ex vivo palmitate storage, acyl-CoA synthetase (ACS) and diacylglycerol-acyltransferase (DGAT) activities, and CD36 protein. Total GPAT and GPAT1 activities decreased as a function of adipocyte size in both omental ( r = −0.71, P = 0.003) and subcutaneous ( r = −0.58, P = 0.04) fat. The relative contribution of GPAT1 to total GPAT activity increased as a function of adipocyte size, accounting for up to 60% of GPAT activity in those with the largest adipocytes. We found strong, positive correlations between ACS, GPAT, and DGAT activities for both sexes and depots ( r values 0.58–0.91) and between these storage factors and palmitate storage rates into TAG ( r values 0.55–0.90). We conclude that: 1) total GPAT activity decreases as a function of adipocyte size; 2) GPAT1 can account for over half of adipose GPAT activity in hypertrophic obesity; and 3) ACS, GPAT, and DGAT are coordinately regulated.

The Esterification of Exogenous Fatty Acids by Adipose Tissue of Hypertriglyceridaemic Subjects with or without Diabetes Mellitus

1976 ◽  
Vol 51 (3) ◽  
pp. 257-265
Author(s):  
P. Clifton-Bligh ◽  
D. J. Galton
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Diabetic Patients ◽  
Adipocyte Size ◽  
Triglyceride Content ◽  
Plasma Insulin Levels ◽  
Fasting Plasma Insulin ◽  
The Difference

1. The esterification of exogenous palmitate to diglyceride and triglyceride in adipocytes was studied in obese and diabetic patients with and without hypertriglyceridaemia. The rate of esterification correlated significantly with the triglyceride content of adipocytes. 2. In diabetic patients with hypertriglyceridaemia, the rate of esterification to triglyceride was significantly greater than in diabetic patients with normotriglyceridaemia. This difference could not be attributed to differences in glucose tolerance or to the degree of obesity. 3. Fasting plasma insulin levels were greater in the hypertriglyceridaemic group than in the normotriglyceridaemic group. The difference in esterification rates could have been due to differences in adipocyte size. 4. The esterification of fatty acid in adipose tissue of diabetic patients was lower than in non-diabetic subjects and this difference could not be accounted for by differences in adipocyte size or differences in the intracellular pools of fatty acid in adipose tissue. 5. The role of esterification of exogenous fatty acids in adipose tissue as a possible determinant of the uptake of glyceride fatty acids from plasma is discussed.

Identification of Markers that Distinguish Adipose Tissue and Glucose and Insulin Metabolism using a Multi-Modal Machine Learning Approach

2021 ◽  
Author(s):  
Josefin Henninger ◽  
Björn Eliasson ◽  
Ulf Smith ◽  
Aidin Rawshani
Keyword(s):  
Machine Learning ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Sphingolipid Metabolism ◽  
Learning Approach ◽  
Adipocyte Size ◽  
Beta Oxidation ◽  
Insulin Metabolism ◽  
Machine Learning Approach

Abstract Background The study of metabolomics has improved our knowledge of the biology behind type 2 diabetes and its related metabolic dysregulations. We aimed to investigate markers of adipose tissue morphology dysfunction and insulin and glucose metabolism dysfunction in 53 non-obese male individuals.Methods The participants underwent extensive clinical, biochemical and magnetic resonance imaging phenotyping, and we also investigated non-targeted serum metabolites. We used a multi-modal machine learning approach to evaluate which serum metabolomic compounds predicted markers of glucose and insulin metabolism, adipose tissue morphology and distribution.Results Fasting glucose was associated with metabolites of intracellular insulin action and beta cell dysfunction, namely cysteine-s-sulphate and n-acetylgarginine. Fasting insulin was predicted by eugenol, a metabolite of beta-oxidation of fatty acids. OGTT glucose levels at 30 minutes were predicted by 7-Hoca and taurochenodeoxycholate, microbiota derived metabolites, as well as, fatty acid chains. Both insulin clamp and HOMA-IR were predicted by metabolites involved in beta-oxidation of fatty acids and biodegradation of triacylglycerol, namely tartrate and 3-phosphoglycerate, as well as pyruvate. OGTT glucose area under curve (AUC) was associated with bile acid metabolites and OGTT insulin AUC was predicted by subcutaneous adipocyte size as well as a metabolite of sphingolipid metabolism. Finally, subcutaneous adipocyte size was associated with several long chain fatty acids, metabolites involved in fatty acid biosynthesis, markers of beta-oxidation of fatty acids, as well as markers of sphingolipid metabolism. Lipid oxidation metabolites also predicted liver lipid accumulation, and cardiac lipid storage was predicted by a metabolite of branched chain amino acid (BCAA) turnover. Only adipocyte cell size, age and alpha-tocopherol were associated with visceral fat.Conclusions We identified several biomarkers associated with markers of dysfunction in adipose tissue and insulin and glucose metabolism using a multi-modal machine learning approach. Our approach demonstrated the relative importance of serum metabolites and they outperformed traditional clinical and biochemical variables for most endpoints.

Schistosomiasis

2010 ◽  
pp. 1202-1212
Author(s):  
D.W. Dunne ◽  
B.J. Vennervald
Keyword(s):  
Life Cycle ◽  
Middle East ◽  
South America ◽  
East Asia ◽  
Fresh Water ◽  
Freshwater Snail ◽  
Snail Host ◽  
Vertebrate Host ◽  
South East Asia ◽  
Intact Skin

Schistosomiasis is caused by trematode worms Schistosoma spp., whose life cycle requires a definitive vertebrate host and an intermediate freshwater snail host. Transmission to humans occurs through exposure to fresh water containing infectious larvae, which can penetrate intact skin before developing into blood-dwelling adult worms. The disease is patchily distributed in parts of South America, Africa, the Middle East, China, and South East Asia, with about 200 million people infected and 20 million suffering severe consequences of infection....

scholarly journals Single-cell analysis of insulin-regulated fatty acid uptake in adipocytes

2010 ◽  
Vol 299 (3) ◽  
pp. E486-E496 ◽  
Author(s):  
Oleg Varlamov ◽  
Romel Somwar ◽  
Anda Cornea ◽  
Paul Kievit ◽  
Kevin L. Grove ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Single Cell ◽  
Cell Size ◽  
Insulin Response ◽  
Fatty Acid Uptake ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Adipocyte Size

Increased body fat correlates with the enlargement of average fat cell size and reduced adipose tissue insulin sensitivity. It is currently unclear whether adipocytes, as they accumulate more triglycerides and grow in size, gradually become less insulin sensitive or whether obesity-related factors independently cause both the enlargement of adipocyte size and reduced adipose tissue insulin sensitivity. In the first instance, large and small adipocytes in the same tissue would exhibit differences in insulin sensitivity, whereas, in the second instance, adipocyte size per se would not necessarily correlate with insulin response. To analyze the effect of adipocyte size on insulin sensitivity, we employed a new single-cell imaging assay that resolves fatty acid uptake and insulin response in single adipocytes in subcutaneous adipose tissue explants. Here, we report that subcutaneous adipocytes are heterogeneous in size and intrinsic insulin sensitivity. Whereas smaller adipocytes respond to insulin by increasing lipid uptake, adipocytes with cell diameters larger than 80–100 μm are insulin resistant. We propose that, when cell size approaches a critical boundary, adipocytes lose insulin-dependent fatty acid transport. This negative feedback mechanism may protect adipocytes from lipid overload and restrict further expansion of adipose tissue, which leads to obesity and metabolic complications.

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