What is HOMA and How to usde it? March 21, 2018

The HOMA model has proved be a robust clinical and epidemiological tool in descriptions of the pathophysiology of diabetes. Already quoted in >500 publications, it has become one of the standard tools in the armamentarium of the clinical physiologist.
 Use and Abuse of HOMA Modeling
by Tara M. Wallace, MD, 
Jonathan C. Levy, MD and 
David R. Matthews, MD
 https://www.sciencedaily.com/releases/2018/03/180320084350.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fhealth_medicine%2Fdiabetes+%28Diabetes+News+--+ScienceDaily%29

So, what is "HOMA" and how this model describe pathology of diabetes and diabetes type 2 particularly?

Homeostatic model assessment (HOMA) of β-cell function and insulin resistance (IR) was first described in 1985 (1). The technique is a method for assessing β-cell function and IR from basal glucose and insulin or C-peptide concentrations. The model has been widely used since it was first published, and we present here an overview of the model and its appropriate use and limitations in clinical science.

So, HOMA is method used to assess function of insulin secreting B-Cells in responce to glucose and insulin concentration.
Now the question, is beta-cells function depend solo on glucose and insulin concentration? 

 The HOMA model is used to yield an estimate of insulin sensitivity and β-cell function from fasting plasma insulin and glucose concentrations (1). The relationship between glucose and insulin in the basal state reflects the balance between hepatic glucose output and insulin secretion, which is maintained by a feedback loop between the liver and β-cells (3). The predictions used in the model arise from experimental data in humans and animals. The β-cell response curve (Fig. 1A) was originally constructed on the basis of a basal production rate of 10 mU/min (74 pmol/min) (4) at a plasma glucose level of 4 mmol/l, into an insulin space of 13 l with a plasma insulin half-life of 4 min (5). Hepatic glucose efflux and uptake are modeled to be dependent on plasma glucose and insulin concentrations (Fig. 1B) (6). Insulin is modeled to decay with a half-life of 3.8 min with an additional slower component (5,7); the insulin concentration controls glucose uptake in fat and muscle (Fig. 1C and D). The basal glucose efflux of 0.8 mmol/min (8,9) is assumed to enter a space of 17 l (9,10). In normal humans, 50% of the basal glucose turnover is to the nervous system, and this is a glucose-dependent process (Fig. 1E) (11). The remainder of glucose uptake by muscle (12–14) and fat is both glucose and insulin dependent (Fig. 1C and D) (15).

      I hope every one understand what authors talking about. I did not. What I do see from all these modeling that they use own fantasy and create fiction how b-cells react on food we eat. It is fantasy, nothing real. As I read in the conclusion, 500 publications were addressed to this model. Is this model clear to understand?
     Insulin resistance is the medical condition when dose of injected insulin is higher then 200 units. Where insulin go? Also it is very wide spread definition of diabetes type 2 that our body system does not use insulin properly. So, how our body system use insulin? Of probably there is no insulin to be used for proper diabetic's needs? Does this HOMA model answer to this questions? Not at all.

In normal humans, 50% of the basal glucose turnover is to the nervous system, and this is a glucose-dependent process

 Based on what this statement published? Is there some prove how glucose used? Finally, what nervous system doing with glucose turned over to it?
     The system and technique which used to create model created solo for one task, to show that it is very difficult to understand, only pro can do it. In reality, no one can understand this model. This model has no meaning. This is why it is never used to diagnose insulin resistance.There are words, and they connected in the mean-less sentences, but regardless of concentration of this words and numbers, meaning is not developed. 
HOMA1-IR = (FPI × FPG)/22.5 HOMA1-%B = (20 × FPI)/(FPG − 3.5)
for IR and β-cell function, respectively, where FPI is fasting plasma insulin concentration (mU/l) and FPG is fasting plasma glucose (mmol/l).

( HOMA - IR)  = X  because we do not know w
 FPI - fasting Insulin Concentration - A
FPG - fasting Plasma Glucose - B
IR - Insulin Resistance - X
B-cell function - Y
  From this formula no one can find meaning of IR or HOMA.  No meaning in all formula.
 

 Very fancy Fantasy, I will say.
OK, Interesting, if someone will really read all this crap? All these fantasy remind me Pr. R. Taylor, how he looks thoughtfully on MRI image and study Beta Cells function. No one can see any beta cells on MRI image, but Pr. R. Taylor see all of them. He is one of those who will take a look at the telescope and see all viruses on Mars. Very smart man.

via Ravenvoron