In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Arachidonic acid (with its precursor – linoleic acid) serve as a substrate to the production of inflammatory mediators known as eicosanoids, whereas the arachidonic acid-containing compound diacylglycerol (DAG) is a precursor to the endocannabinoid 2-arachidonoylglycerol (2-AG) while fatty acid amide hydrolase (FAAH) mediates the metabolism of anandamide into arachidonic acid. Anandamide can also be produced from N-acylphosphatidylethanolamine via several pathways. Anandamide and 2-AG can also be hydrolized into arachidonic acid, potentially leading to increased eicosanoid synthesis. Metabolic syndrome is a risk factor for neurological disorders. Metabolomic studies suggest an excess of organic acids, impaired lipid oxidation byproducts, essential fatty acids and essential amino acids in the blood serum of affected patients.
The pathogenesis of essential hypertension is multifactorial and complex.  Multiple factors modulate the blood pressure (BP) including humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute, the exact mechanisms underlying essential hypertension have not been established.
Okay, you've suffered through the particulars and are sufficiently MRT-educated. Let's get to the good stuff: three tried-and-true MRT strategies guaranteed to help strip away stubborn fat and heighten acid-buffering ability. You can stick with one strategy for a given timeframe or periodize strategies from one week to the next. Regardless of what you decide to do, it's best to insert an "unloading microcycle" (one week of light weight) every fourth week or so to avoid the potential for overtraining. During the unloading cycle, reduce the effort expended so you're not substantially challenging your muscles on the last few reps of each set (aim for about a 7 on an RPE scale of 1-10). As a general rule, limit metabolic training cycles to a maximum of about 8 weeks. Any longer and you risk compromising muscular gains.
[Guideline] Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018 Jun. 71(6):e13-e115. [Medline]. [Full Text].