While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight.
Metabolic syndrome is a burgeoning global problem. Approximately one fourth of the adult European population is estimated to have metabolic syndrome, with a similar prevalence in Latin America.  It is also considered an emerging epidemic in developing East Asian countries, including China, Japan, and Korea. The prevalence of metabolic syndrome in East Asia may range from 8-13% in men and from 2-18% in women, depending on the population and definitions used. [29, 30, 31]
Metabolic syndrome is a multiplex risk factor that arises from insulin resistance accompanying abnormal adipose deposition and function.  It is a risk factor for coronary heart disease, as well as diabetes, fatty liver, and several cancers. The clinical manifestations of this syndrome may include hypertension, hyperglycemia, hypertriglyceridemia, reduced high-density lipoprotein cholesterol (HDL-C), and abdominal obesity. (See Prognosis, Workup, Treatment, and Medication.)
^ Sattar N, Preiss D, Murray HM, Welsh P, Buckley BM, de Craen AJ, Seshasai SR, McMurray JJ, Freeman DJ, Jukema JW, Macfarlane PW, Packard CJ, Stott DJ, Westendorp RG, Shepherd J, Davis BR, Pressel SL, Marchioli R, Marfisi RM, Maggioni AP, Tavazzi L, Tognoni G, Kjekshus J, Pedersen TR, Cook TJ, Gotto AM, Clearfield MB, Downs JR, Nakamura H, Ohashi Y, Mizuno K, Ray KK, Ford I (February 2010). "Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials". Lancet. 375 (9716): 735–42. doi:10.1016/S0140-6736(09)61965-6. PMID 20167359.
When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego. http://www.sandysidhumedia.com/wp-content/uploads/2012/12/angelaquote1.jpg
When it comes to laboratory values, numbers like blood glucose and A1C levels are commonly checked. Less often, doctors order a test for your fasting insulin level; yet this test can help predict your risk of developing prediabetes and metabolic syndrome. Insulin plays a key role in metabolism, and high insulin levels can promote obesity, stimulate hunger, and increase the storage of fat.
Metabolic syndrome is similarly prevalent in men (24%) and women (22%), after adjusting for age.  However, several considerations are unique to women with metabolic syndrome, including pregnancy, use of oral contraceptives, and polycystic ovarian syndrome.  Metabolic syndrome and polycystic ovarian syndrome share the common feature of insulin resistance; they therefore share treatment implications as well.  Cardiometabolic risk is thought to be elevated in both groups. 
The United Kingdom Prospective Diabetes Study (UKPDS) was a clinical study conducted by Z that was published in The Lancet in 1998. Around 3,800 people with type 2 diabetes were followed for an average of ten years, and were treated with tight glucose control or the standard of care, and again the treatment arm had far better outcomes. This confirmed the importance of tight glucose control, as well as blood pressure control, for people with this condition.
Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered. https://www.lorilynnsmith.com/wordpress/wp-content/uploads/2012/04/2012-04-30_2116.png
Secondary hypertension can be caused by kidney disease; sleep apnea; coarctation of the aorta; disease of the blood vessels supplying the kidneys; various endocrine gland disorders; the use of oral contraceptives; smoking; alcohol intake of more than two drinks per day; chronic use of non-steroidal anti-inflammatory drugs (NSAIDs); and antidepressant use.
One of the most common ways people with type 2 diabetes attempt to lower their blood sugar is by drastically reducing their intake of carbs. The ADA agrees that carbohydrate counting is essential if you have diabetes, but extreme diets like the ketogenic diet, which reduces carb intake to as little as 5 percent of your daily calories, can be risky for some people with diabetes. (36)
Jock itch is an itchy red rash that appears in the groin area. The rash may be caused by a bacterial or fungal infection. People with diabetes and those who are obese are more susceptible to developing jock itch. Antifungal shampoos, creams, and pills may be needed to treat fungal jock itch. Bacterial jock itch may be treated with antibacterial soaps and topical and oral antibiotics.
Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.
Even the low-fat craze that kicked off in the late 1970s–which was based on the intuitively appealing but incorrect notion that eating fat will make you fat–depended on the calorie-counting model of weight loss. (Since fatty foods are more calorie-dense than, say, plants, logic suggests that if you eat less of them, you will consume fewer calories overall, and then you’ll lose weight.)
You can take additional magnesium if you do not think you’re getting enough in the diet. Dr. Weil recommends magnesium citrate, chelate, or glycinate. Avoid magnesium oxide, which can be irritating, and take half the amount of magnesium as the calcium you take in supplemental form. If you do not take any supplemental calcium, watch out for taking large amounts of magnesium, which can cause diarrhea.
There is no known preventive measure for type 1 diabetes. Type 2 diabetes – which accounts for 85–90% of all cases – can often be prevented or delayed by maintaining a normal body weight, engaging in physical activity, and consuming a healthy diet. Higher levels of physical activity (more than 90 minutes per day) reduce the risk of diabetes by 28%. Dietary changes known to be effective in helping to prevent diabetes include maintaining a diet rich in whole grains and fiber, and choosing good fats, such as the polyunsaturated fats found in nuts, vegetable oils, and fish. Limiting sugary beverages and eating less red meat and other sources of saturated fat can also help prevent diabetes. Tobacco smoking is also associated with an increased risk of diabetes and its complications, so smoking cessation can be an important preventive measure as well.
First-line medications for hypertension include thiazide-diuretics, calcium channel blockers, angiotensin converting enzyme inhibitors (ACE inhibitors), and angiotensin receptor blockers (ARBs). These medications may be used alone or in combination (ACE inhibitors and ARBs are not recommended for use in combination); the latter option may serve to minimize counter-regulatory mechanisms that act to restore blood pressure values to pre-treatment levels. Most people require more than one medication to control their hypertension. Medications for blood pressure control should be implemented by a stepped care approach when target levels are not reached.
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.
Though the above guidelines are important, they are not the only hypertension guidelines and currently there is no consensus on them. In 2014, experts appointed to the Eighth Joint National Committee (JNC 8) proposed a different set of guidelines and blood pressure goals and some physician groups continue to endorse these recommendations. The table below summarizes the new goals or target blood pressure readings for specific populations:
Emerging data suggest an important correlation between metabolic syndrome and risk of stroke.  Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke.  Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators.