Lipodystrophy: Syndrome of severe insulin resistance

Bindlish, Shagun; Presswala, Lubaina; Schwartz, Frank

doi:10.1080/00325481.2015.1015927

Cited by 30 publications

(22 citation statements)

References 29 publications

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“…We identified two unrelated individuals with NPS. We examined their glucose and insulin homeostasis status, since both partial and generalized lipodystrophic disorders are frequently associated with insulin resistance (Bindlish et al, 2015). Contrary to this notion, overnight-fasted plasma insulin levels from our NPS patients were 2-fold lower than unaffected subjects, while maintaining euglycemia (Figure 1A).…”

Section: Resultsmentioning

confidence: 99%

Asprosin, a Fasting-Induced Glucogenic Protein Hormone

Romere

Duerrschmid

Bournat

et al. 2016

Cell

422

675

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SUMMARY Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.

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Section: Resultsmentioning

confidence: 99%

Asprosin, a Fasting-Induced Glucogenic Protein Hormone

Romere

Duerrschmid

Bournat

et al. 2016

Cell

422

675

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“…This remodeling is characterized by an inflammatory response with immune cell migration, proliferation of the cellular components of the SVF, and changes in ECM of AT [5]. Intense research during the past two decades has characterized AT remodeling in human diseases that exhibit high AT lipolysis rates, such as obesity [5, 74], metabolic syndrome [75], and lipodystrophy [76]. More recently, different aspects of AT remodeling in dairy cows during the transition period and metabolic disease were evaluated.…”

Section: Adipose Tissue Remodelingmentioning

confidence: 99%

Adipose tissue lipolysis and remodeling during the transition period of dairy cows

Contreras

Strieder‐Barboza

Raphael

2017

J Animal Sci Biotechnol

128

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Elevated concentrations of plasma fatty acids in transition dairy cows are significantly associated with increased disease susceptibility and poor lactation performance. The main source of plasma fatty acids throughout the transition period is lipolysis from adipose tissue depots. During this time, plasma fatty acids serve as a source of calories mitigating the negative energy balance prompted by copious milk synthesis and limited dry matter intake. Past research has demonstrated that lipolysis in the adipose organ is a complex process that includes not only the activation of lipolytic pathways in response to neural, hormonal, or paracrine stimuli, but also important changes in the structure and cellular distribution of the tissue in a process known as adipose tissue remodeling. This process involves an inflammatory response with immune cell migration, proliferation of the cellular components of the stromal vascular fraction, and changes in the extracellular matrix. This review summarizes current knowledge on lipolysis in dairy cattle, expands on the new field of adipose tissue remodeling, and discusses how these biological processes affect transition cow health and productivity.

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“…Further, transplanting insulin sensitive adipose tissue into insulin resistance animals restores insulin responsiveness (68)(69)(70). Finally, overt lack of adipose tissue function is sufficient to induce insulin resistance (71). Therefore adipose tissue may be the dominant regulator of whole-body insulin sensitivity.…”

Section: Further Insulin Resistance and Adiposity Fail To Correlate mentioning

confidence: 99%

Adipocyte JAK2 Mediates Growth Hormone-Induced Hepatic Insulin Resistance

Corbit

Camporez²,

Tran

et al. 2016

Preprint

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For nearly 100 years, Growth Hormone (GH) has been known to regulate insulin sensitivity and risk of diabetes. However, the tissue governing the effects of GH signaling on insulin and glucose homeostasis remains unknown. Excess GH reduces fat mass and insulin sensitivity. Conversely, GH insensitivity (GHI) is associated with increased adiposity, augmented insulin sensitivity, and protection from diabetes.Here we induce adipocyte-specific GHI through conditional deletion of Jak2 (JAK2A), an obligate transducer of GH signaling. Similar to whole-body GHI, JAK2A mice had increased adiposity and extreme insulin sensitivity. Loss of adipocyte Jak2 augmented hepatic insulin sensitivity and conferred resistance to diet-induced metabolic stress without overt changes in circulating fatty acids. While GH injections induced hepatic insulin resistance in control mice, the diabetogenic action was absent in JAK2A mice. Collectively, our results show that adipose tissue governs the effects of GH on insulin and glucose homeostasis. Further, we show that JAK2 mediates liver insulin sensitivity via an extra-hepatic, adipose tissue-dependent mechanism.

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Lipodystrophy: Syndrome of severe insulin resistance

Cited by 30 publications

References 29 publications

Asprosin, a Fasting-Induced Glucogenic Protein Hormone

Asprosin, a Fasting-Induced Glucogenic Protein Hormone

Adipose tissue lipolysis and remodeling during the transition period of dairy cows

Adipocyte JAK2 Mediates Growth Hormone-Induced Hepatic Insulin Resistance

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