There are some interesting developments in blood glucose monitoring including continuous glucose sensors. The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. This cannula allows for frequent sampling of blood glucose levels. Attached to this is a transmitter that sends the data to a pager-like device. This device has a visual screen that allows the wearer to see, not only the current glucose reading, but also the graphic trends. In some devices, the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. One version is specifically designed to interface with their insulin pumps. In most cases the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives, it can only give a calculated suggestion as to whether the wearer should give insulin, and if so, how much). However, in 2013 the US FDA approved the first artificial pancreas type device, meaning an implanted sensor and pump combination that stops insulin delivery when glucose levels reach a certain low point. All of these devices need to be correlated to fingersticks measurements for a few hours before they can function independently. The devices can then provide readings for 3 to 5 days.
The second hormone that becomes involved when you begin to lose weight is a hormone known as leptin. Leptin is a hormone that is released from the fat cells to signal to the brain about how much fat we have in storage. To our body this is kind of like the indicator on a car telling us how much fuel we have in the tank. Leptin is also a messenger that is involved with controlling your metabolic rate AND your appetite.
The distribution of adipose tissue appears to affect its role in metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of potential explanations for this, including experimental observations that omental fat is more resistant to insulin and may result in a higher concentration of toxic free fatty acids in the portal circulation. [21]
Adapted from:  Chobanian AV, Bakris GL, Black HR, et al, and the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. Dec 2003;42(6):1206-52. [2]

Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization (WHO) when the current taxonomy was introduced in 1999.[53]
Investigations into the pathophysiology of hypertension, both in animals and humans, have revealed that hypertension may have an immunological basis. Studies have revealed that hypertension is associated with renal infiltration of immune cells and that pharmacologic immunosuppression (such as with the drug mycophenolate mofetil) or pathologic immunosuppression (such as occurs with HIV) results in reduced blood pressure in animals and humans. Evidence suggests that T lymphocytes and T-cell derived cytokines (eg, interleukin 17, tumor necrosis factor alpha) play an important role in hypertension. [14, 15]
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.[37][35] Anandamide can also be produced from N-acylphosphatidylethanolamine via several pathways.[35] Anandamide and 2-AG can also be hydrolized into arachidonic acid, potentially leading to increased eicosanoid synthesis.[35] Metabolic syndrome is a risk factor for neurological disorders.[38] 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.

Despite these genetic findings, targeted genetic therapy seems to have little impact on hypertension. In the general population, not only does it appear that individual and joint genetic mutations have very small effects on BP levels, but it has not been shown that any of these genetic abnormalities are responsible for any applicable percentage of cases of hypertension in the general population. [27]

^ Vancampfort D, Correll CU, Wampers M, Sienaert P, Mitchell AJ, De Herdt A, Probst M, Scheewe TW, De Hert M (July 2014). "Metabolic syndrome and metabolic abnormalities in patients with major depressive disorder: a meta-analysis of prevalences and moderating variables". Psychological Medicine. 44 (10): 2017–28. doi:10.1017/S0033291713002778. PMID 24262678.
This explains why my attempts at a low fat, high protein, high carb diet left me gaining weight all while eating 1000 calories per day! Those 1000 calories were simply fueling my brain and then getting shuttled into my fat cells. If you are not insulin resistant, then this diet may be just the thing you need to shed some short term pounds (although I never recommend a 1000 calorie diet!- more on that later), but to me it caused metabolic chaos.
Grab the bar with a shoulder-width, underhand grip, and hang at arm's length. You should return to this position each time you lower your body back down. Perform a chin-up by taking 1 second to pull your collarbone to the bar. As you pull your body up, stick your chest out, squeeze your shoulder blades down and back, and focus on pulling your upper arms down forcefully. Once the top of your chest touches the bar, pause, then take 3 seconds to lower your body back to a dead hang. That's 1 rep.

^ Sacks, F. M.; Svetkey, L. P.; Vollmer, W. M.; Appel, L. J.; Bray, G. A.; Harsha, D.; Obarzanek, E.; Conlin, P. R.; Miller, E. R. (2001-01-04). "Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group". The New England Journal of Medicine. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. ISSN 0028-4793. PMID 11136953.
^ Jump up to: a b Go, AS; Bauman, M; King, SM; Fonarow, GC; Lawrence, W; Williams, KA; Sanchez, E (15 November 2013). "An Effective Approach to High Blood Pressure Control: A Science Advisory From the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention". Hypertension. 63 (4): 878–85. doi:10.1161/HYP.0000000000000003. PMID 24243703. Archived from the original on 20 November 2013. Retrieved 20 November 2013.