Hypoparathyroidism.

Hypoparathyroidism is a rare endocrine disease caused by an absence or insufficient production of parathormone. Parathormone deficiency leads to lower serum calcium concentration that is responsible for patients' neuromuscular symptoms. Conventional treatment consists of calcium and active vitamin D metabolites administration but doesn't constitute an adequate substitution of missing parathormone. Although the treatment substantially alleviates patients' troubles, chronic complications may develop because of hyperphosphatemia and conventional medication. Solution to this resides in recombinant parathormone administration, however the only one drug available is being now recalled from the market. The mainstay of hypoparathyroidism prevention is the judicious indication of total thyroidectomy representing the main cause of the disease.

Regulation of blood flow in adipose tissue: involvement of the cholinergic system.

Acetylcholine (Ach) has vasodilatory actions. However, data are conflicting about the role of Ach in regulating blood flow in subcutaneous adipose tissue (ATBF). This may be related to inaccurate ATBF recording or to the responder/nonresponder (R/NR) phenomenon. We showed previously that healthy individuals are R (ATBF increases postprandially by >50% of baseline BF) or NR (ATBF increases ≤50% postprandially). Our objective was to assess the role of the cholinergic system on ATBF in R and NR subjects. ATBF was manipulated by in situ microinfusion of vasoactive agents (VA) in AT and monitored by the (133)Xenon washout technique (both recognized methods) at the VA site and at the control site. We tested incrementally increasing doses of Ach (10(-5), 10(-3), and 10(-1) mol/l; n = 15) and Ach receptor antagonists (Ra) before and after oral administration of 75-g glucose using atropine (muscarinic Ra; 10(-4) mol/l, n = 13; 10(-5) mol/l, n = 22) and mecamylamine (nicotinic Ra; 10(-3) mol/l, n = 15; 10(-4) mol/l, n = 10). Compared with baseline [2.41 (1.36-2.83) ml·100 g(-1)·min(-1)], Ach increased ATBF dose dependently [3.32 (2.80-5.09), 6.46 (4.36-9.51), and 10.31 (7.98-11.52), P < 0.0001], with no difference between R and NR. Compared with control side, atropine (both concentrations) had no effect on fasting ATBF; only atropine 10(-4) mol/l decreased post-glucose ATBF [iAUC: 1.25 (0.32-2.91) vs. 1.98 (0.64-2.94); P = 0.04]. This effect was further apparent in R. Mecamylamine had no impact on fasting and postglucose ATBF in R and NR. Our results suggest that the cholinergic system is implicated in ATBF regulation, although it has no role in the blunting of ATBF response in NR.

Measurement and manipulation of human adipose tissue blood flow using xenon washout technique and adipose tissue microinfusion.

Adipose tissue (AT) is a very active organ, both metabolically and hormonally. These important functions depend on adequate blood flow (BF). Metabolic, hormonal, and vascular processes within AT are highly interconnected and any disruption will invariably impact the others. Therefore, any alteration of ATBF with obesity and/or insulin resistance will impact metabolic and hormonal AT functions. Similarly, metabolic or hormonal changes in AT will lead to ATBF disturbance. Thus, it is plausible that insufficient ATBF alters AT metabolic processes and response to regulatory signals, and may even aggravate the negative impacts of dysfunction in AT. The role of BF in AT metabolism can be evaluated by several techniques, but the xenon washout method is considered the "gold" standard. This technique can be combined with local microinfusion protocols, and the combination allows for precise assessment of mechanisms implicated in ATBF regulation.

Update on adipose tissue blood flow regulation.

According to Fick's principle, any metabolic or hormonal exchange through a given tissue depends on the product of the blood flow to that tissue and the arteriovenous difference. The proper function of adipose tissue relies on adequate adipose tissue blood flow (ATBF), which determines the influx and efflux of metabolites as well as regulatory endocrine signals. Adequate functioning of adipose tissue in intermediary metabolism requires finely tuned perfusion. Because metabolic and vascular processes are so tightly interconnected, any disruption in one will necessarily impact the other. Although altered ATBF is one consequence of expanding fat tissue, it may also aggravate the negative impacts of obesity on the body's metabolic milieu. This review attempts to summarize the current state of knowledge on adipose tissue vascular bed behavior under physiological conditions and the various factors that contribute to its regulation as well as the possible participation of altered ATBF in the pathophysiology of metabolic syndrome.

[Adipose tissue blood flow and metabolic syndrome]. / Prutok krve tukovou tkání a metabolický syndrom.

Worldwide growth of obesity and prevalence of type 2 diabetes mellitus reach the extent of a pandemy and represent a considerable medical and economic problem. An attention devoted to adipose tissue has led to the shift in general perception of its importance. It becomes evident that adipose tissue is not by far only an energy store with thermal and mechanical protection of other organs and body. A number of important functions in intermediary metabolism and hormonal interactions with other tissues have been disclosed. Metabolic flexibility of adipose tissue represents an essential protection against undesirable effects of excessive energy intake. Nevertheless, after exceeding of its physiological capacity adipose tissue becomes an important cause of insulin resistance, oxidative stress and a number of other derangements leading to atherosclerosis progression and increase of cardiovascular morbidity and mortality. Not only adipocytes but also stromal cells and vascular bed participate in the physiological and pathological functions of adipose tissue. Adequate regulation of adipose tissue blood flow ensures communication with other systems and appropriate reactions to energy needs of the organism. Disturbances in adipose tissue blood flow evolve at early stages of obesity and participate in the worsening of metabolic syndrome.