Clinica Chimica Acta Volume 419, 18 April 2013, Pages 87–94

White adipose tissue is recognized as a dynamic endocrine organ able to produce and release several bioactive polypeptides known as adipokines. Obesity is defined as an excessive growth of adipose tissue. As such, it is likely that adipokines could play an important role in the development of diseases associated with obesity including insulin resistance, inflammation, hypertension, cardiovascular risk and metabolic disorders. This review focuses on obesity specific-adipokine profiles and the role of some adipokines in obesity-related metabolic disorders.

Highlights

► Obesity is defined as an excessive growth of adipose tissue. ► White adipose tissue expresses and secretes several bioactive polypeptides, known as adipokines. ► In the obese state, adipokines play a central role in the developing of obesity-related metabolic disorders.

Endocrine Reviews 2009; 31 (1): 1-24

Obesity has become a serious public health problem and a major risk factor for the development of illnesses, such as insulin resistance and hypertension. Human homeostatic systems have adapted to daily changes in light and dark in a way that the body anticipates the sleep and activity periods. Mammals have developed an endogenous circadian clock located in the suprachiasmatic nuclei of the anterior hypothalamus that responds to the environmental light-dark cycle. Similar clocks have been found in peripheral tissues, such as the liver, intestine, and adipose tissue, regulating cellular and physiological functions. The circadian clock has been reported to regulate metabolism and energy homeostasis in the liver and other peripheral tissues. This is achieved by mediating the expression and/or activity of certain metabolic enzymes and transport systems. In return, key metabolic enzymes and transcription activators interact with and affect the core clock mechanism. In addition, the core clock mechanism has been shown to be linked with lipogenic and adipogenic pathways. Animals with mutations in clock genes that disrupt cellular rhythmicity have provided evidence for the relationship between the circadian clock and metabolic homeostasis. In addition, clinical studies in shift workers and obese patients accentuate the link between the circadian clock and metabolism. This review will focus on the interconnection between the circadian clock and metabolism, with implications for obesity and how the circadian clock is influenced by hormones, nutrients, and timed meals.

I. Introduction

II. Circadian Rhythms
A. Circadian rhythms in mammals
B. Circadian rhythms, well-being, and life span

III. The Biological Clock
A. The location of the mammalian biological clock
B. The biological clock at the molecular level
C. Circadian rhythms in peripheral clocks

IV. The Biological Clock and Energy Homeostasis
A. SCN efferents
B. SCN afferents
C. Effect of neuropeptides and hormones on SCN
D. Circadian rhythms and metabolism
E. Effect of metabolism on circadian rhythms
F. Effect of feeding regimens on circadian rhythms

V. The Biological Clock and Obesity
A. SCN connection to adipose tissue
B. Effect of circadian rhythms on lipid metabolism
C. Effect of high-fat diet on circadian rhythms
D. Circadian rhythms and body weight
E. Clock mutations and metabolic disorders
F. Sleep, shift work, and obesity
VI. Summary and Conclusions

Clinical Chemistry. 2008;54:945-955

Background: As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects.

Content: In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic &豪-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact.

Summary: Adipocyte endoplasmic reticulum and mitochondrial stress, and associated changes in circulating adipokines, free fatty acids, and inflammatory mediators, are central to adverse health effects of adiposity. Future investigation should focus on these pathways and on reversing the adverse lifestyle behaviors that are the fundamental causes of adiposity.

Hacettepe Tıp Derg 2007;38:167-172

Obezite, vücudun gereksiniminden fazla enerji içeren gıda alımı nedeniyle yağ dokusu oranında artış olması ve bunun sonucunda da vücut ağırlığının artması olarak tanımlanmaktadır. Vücut ağırlığında artış, vücut kitle indeksi (VKİ)’nde de artışa sebep olur. VKİ > 30 olması durumunda kişi obez olarak değerlendirilir. Obezite bugün, yol açtığı komplikasyonlar nedeniyle yaşamı tehdit eden bir durum olarak görülmektedir. En önemli komplikasyonu olan Tip 2 diabetes mellitus (DM) gelişimine yol açmasının yanı sıra, kardiyovasküler hastalıklara ve kansere de zemin hazırlamaktadır. Obezitenin oluşumunda, enerji dengesini düzenleyen nöroendokrin mekanizmalar üzerinde etkili olan çevresel ve genetik faktörlerin rol oynadığı düşünülmektedir. Normal kilodaki insanlar, gereksinimlerinden fazla gıda alımı sonucu vücut yağ depolarının artmasına karşı korunur. Adipozitenin olumsuz geribildirimi olarak tanımlanan bu olgu, yağ kütlesinin artması durumunda iştahın azalacağı ve enerji harcanmasının artacağını öneren lipostat teorisi ile uyumludur. İştahın düzenlenmesi insanlarda santral sinir sistemi düzeyinde olmaktadır ve bu düzenlenmeye aracılık eden başlıca molekül adipositler tarafından üretilen leptindir. Küçük bir protein olan leptin vücut yağ içeriği ile orantılı düzeyde kanda bulunur ve santral sinir sistemine geçer. Leptin reseptörü ekspresyonunun en yüksek olduğu yer bazomedial hipotalamustaki arkuat çekirdektir.