It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNF-α and alter levels of a number of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-α has been shown not only to cause the production of inflammatory cytokines, but also possibly to trigger cell signaling by interaction with a TNF-α receptor that may lead to insulin resistance. An experiment with rats fed a diet with 33% sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance. The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.
^ Jump up to: a b c Giuseppe, Mancia; Fagard, R; Narkiewicz, K; Redon, J; Zanchetti, A; Bohm, M; Christiaens, T; Cifkova, R; De Backer, G; Dominiczak, A; Galderisi, M; Grobbee, DE; Jaarsma, T; Kirchhof, P; Kjeldsen, SE; Laurent, S; Manolis, AJ; Nilsson, PM; Ruilope, LM; Schmieder, RE; Sirnes, PA; Sleight, P; Viigimaa, M; Waeber, B; Zannad, F; Redon, J; Dominiczak, A; Narkiewicz, K; Nilsson, PM; et al. (July 2013). "2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)". European Heart Journal. 34 (28): 2159–219. doi:10.1093/eurheartj/eht151. PMID 23771844.
Forouzanfar MH, Alexander L, Anderson HR, et al, for the GBD 2013 Risk Factors Collaborators. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015 Dec 5. 386 (10010):2287-323. [Medline].
One hypothesis is that prehypertension results in oxidation of lipids such as arachidonic acid that leads to the formation of isoketals or isolevuglandins, which function as neoantigens, which are then presented to T cells, leading to T-cell activation and infiltration of critical organs (eg, kidney, vasculature).  This results in persistent or severe hypertension and end organ damage. Sympathetic nervous system activation and noradrenergic stimuli have also been shown to promote T-lymphocyte activation and infiltration and contribute to the pathophysiology of hypertension. [17, 18, 19]
A blood pressure reading measures both the systolic and diastolic forces, with the systolic pressure listed first. The numbers show your pressure in units of millimeters of mercury (mm Hg)—how high the pressure inside your arteries would be able to raise a column of mercury. For example, a reading of 120/80 mm Hg means a systolic pressure of 120 mm Hg and diastolic pressure of 80 mm Hg.
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the pancreatic islets, leading to insulin deficiency. This type can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, in which a T cell-mediated autoimmune attack leads to the loss of beta cells and thus insulin. It causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults, but was traditionally termed "juvenile diabetes" because a majority of these diabetes cases were found in children.