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Whether having breakfast will help or hinder glucose control will also depend on its macronutrient composition and carbohydrate content. In their 2011 study Pereira et al. were able to show that a high carbohydrate, high GI breakfast will have a similarly negative impact on glucose control of adults and children as having no breakfast at all (Pereira. 2011).

Intermittent fasting (IF), i.e. skipping breakfast and/or other meals in order to stay fasted for ~16h+ per day is no longer "all the rage", but still highly popular among people who believe in its health and weight loss benefits. And in fact, there is some research (also from a couple of Ramadan studies) that appears to confirm the notion that it is healthy and may - even without deliberate caloric restriction - facilitate weight and more importantly fat loss.

On the other hand, intermittent fasting conflicts with everything we've been (falsely?) told about the benefits of frequent meals. Benefits of which waredownloadsoft readers know that they are quasi-non-existent, in most healthy individuals and sometimes even counter-productive in obese and diabetic individuals, where most studies refute that eating more frequently provides significant weight loss benefits in the context of a calorically restricted diet.
Now, a recent study from the Diabetes Unit, Wolfson Medical Center of the Sackler Faculty of Medicine at the Tel Aviv University, the Lund University in Sweden and the Hebrew University of Jerusalem (Jakubowicz. 2015) suggests that extending your overnight fast by skipping breakfast may have real (not just corollary) detrimental effects on habitual breakfast eaters (learn why this is important) who are suffering from type II diabetes (with glycated hemoglobin (HbA1c) levels of 7–9% (the subjects in the study at hand were more than just pre-diabetic).

In this group of subjects, skipping breakfast increases post-prandial hyperglycemia (PPHG) after lunch and dinner. It lowers the important GLP-1 response to the meals (learn more about how GLP-1 is important in "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?") and impairs the subjects' already messed up insulin response. More specifically,

• Three meals may be ok, but six meals are actually counterprodutive in T2DM.

  the lunch AUC0-180 for glucose, FFA, and glucagon were 36.8, 41.1 and 14.8% higher, respectively, and the AUC0-180 for insulin and  iGLP-1 17.0% and 19.0% lower, respectively, on the NoB[reakfast] day compared with the YesB[reakfast] day (P < 0.0001), 
• the dinner AUC0-180 for glucose, FFA, and glucagon were 26.6, 29.6, and 11.5% higher, respectively, and the the AUC0-180 for insulin and iGLP-1 were 7.9% and 16.5% lower on the NoB day compared with the YesB day (P < 0.0001), on the other hand

Whether the conclusion that "[b]reakfast consumption could be a successful strategy for reduction of PPHG [prostprandial hyperglycemia] in type 2 diabetes" applies to every type II diabetic is yet as questionable as the assumption that you could extrapolate the data from this acute phase study and use it to predict the long-term response in diabetics, let alone health individuals.

Figure 2: Hunger, satiety, plasma glucose and insulin in the Eaters and Skippers in the two conditions in Thomas (2015).

If we go back to Thomas' recently published study (I have discussed it in detail here), it is after all obvious that the scientists choice of subjects who consume breakfast regularly may have thwarted their results. I mean, the researchers from the University of Colorado School of Medicine and the Denver Health Medical Center have shown quite conclusively that one's breakfast habits will determine whether skipping breakfast increases insulin, hunger and blood lipids or not.
References:

If you oxidize the CHOs from this meal, instead of storing it as glycogen, that's bad news for ability to maintain your body weight over the next 6-months & beyond

You will know (and maybe hate) them, people who are eating whatever they want, whenever they want while still being not exactly shredded, but at least very lean. What do all these people who have an extremely easy time keeping their weight stable in common?

A recent study from the Phoenix Epidemiology and Clinical Research Branch at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the "glorious" National Institutes of Health (NIH) suggests that it may relate to the way they respond to fasting and overfeeding on high carb, low protein and eucaloric diets.
It is by no means news that there is a considerable inter-individual variation in the energy cost of weight gain. Some people gain weight on a caloric surplus of only 10kcal/day, while others stash away hundreds of extra kcals without gaining a single pound of body fat (these figures have only illustrative values and are not meant to be "exact").

"In a prior cross-sectional study, the increase in energy expenditure (EE) with overfeeding and the decrease with fasting were found to be correlated in a small group of 14 male subjects (Weyer. 2011). Our group has previously shown that the EE response to overfeeding varies considerably among individuals but is consistent and reproducible within individuals. This individual contribution explains more of the observed variability in the EE changes with overfeeding than changes to the macronutrient content of the diet (Thearle. 2013). These studies seem to indicate that phenotypic differences may exist in the EE responses to fasting or overfeeding that may affect susceptibility to weight gain. As overeating or caloric restriction are necessary to alter weight, perturbations in energy balance may be needed to uncover responses that signify an energy conserving physiology versus a physiology that is better able to resist weight gain" (Schlögl. 2015).

In their latest study, Schlögl and colleagues extend their previous findings by addressing the question of whether this inter-individual variation in EE changes relates to future weight change. Or, to put it simply: They tried to answer the question

"Will your acute reaction to 24h overfeeding on different diets predict if you can maintain your weight over the next 6 months, or not?"

To answer the question, the 24-h EE during energy balance during fasting and four different overfeeding diets with 200% energy requirements was measured in a metabolic chamber in 37 subjects with normal glucose regulation while they resided in the clinical research unit of the NIH. Each of the diets was administered for exactly 24h with 3-day washouts in-between (breakfast at 07:00, entry into the calorimeter one hour later; further meals were provided inside the calorimeter at 11:00, 16:00, and 19:00 through a two-door airlock):

• a eucaloric reference diet which was 80% of the weight maintaining diet to account for the reduced energy expenditure due to being confined to the metabolic chamber that contained 50% carbohydrates, 30% fats, and 20% proteins
• a fasting trial (FST) in which the subjects sat in the metabolic chamber fasted
• a low-protein diet (LPF) with 51% carbohydrate, 46% fat, 3% protein
• a standard overfeeding diet (SOF) with 50% carbohydrate, 30% fat, 20% protein
• a high-fat, normal-protein overfeeding diet (FNP) with 20% carbohydrate, 60% fat, 20% protein
• a high-carbohydrate, normal-protein overfeeding diet (CNP) with 75% carbohydrate, 5% fat and 20% protein

To be able to assess the long-term weight gain, all participants returned for follow-up visit to the NIH headquarter 6-months after the initial measures.On that occasion, their body weight and composition (DXA | unfortunately, the body fat level was not analyzed seperately) was measured and the change in body weight was correlated with (a) the decrease in 24-h EE during fasting and (b) the increase with the different overfeeding protocols.

Figure 1: 24h energy expression expressed relative to eucaloric reference diet (Schlögl. 2015)

The results of the scientists' correlation analysis were surprisingly unambiguous: A larger reduction in EE during fasting, a smaller EE response to low-protein overfeeding and a larger response to high-carbohydrate overfeeding all correlated with weight gain.

Figure 2: Sign. correlations between change in 24-EE during overfeeding / fasting and weight gain (Schlögl. 2015).

If you take a closer look at the correlations (r-values) and their significance in Figure 2 you will realize that all of them are statistically significant . In other words, there is a significant link between an increased risk of gaining weight in the next 6 months and

• a higher decrease in energy expenditure during fasting (Figure 2; A | this should remind you of the thrifty phenotype theory, cf. Wells. 2011)
• a smaller increase in energy expenditure during low protein dieting (Figure 2; B)
• a higher increase in energy expenditure during carbohydrate overfeeding (Figure 2; C)
• a higher higher reliance on fat during fasting (Figure 2; D)

References:

• Pannacciulli, Nicola, et al. "The 24-h carbohydrate oxidation rate in a human respiratory chamber predicts ad libitum food intake." The American journal of clinical nutrition 86.3 (2007): 625-632.
• Schlögl, Mathias, et al. "Energy expenditure responses to fasting and overfeeding identify phenotypes associated with weight change." Diabetes (2015): db150382.
• Thearle, Marie S., et al. "Extent and determinants of thermogenic responses to 24 hours of fasting, energy balance, and five different overfeeding diets in humans." The Journal of Clinical Endocrinology & Metabolism 98.7 (2013): 2791-2799.
• Wells, Jonathan CK. "The thrifty phenotype: An adaptation in growth or metabolism?." American Journal of Human Biology 23.1 (2011): 65-75.
• Weyer, C., et al. "Changes in energy metabolism in response to 48 h of overfeeding and fasting in Caucasians and Pima Indians." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 25.5 (2001): 593-600.
• Zurlo, Francesco, et al. "Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ." American Journal of Physiology-Endocrinology And Metabolism 259.5 (1990): E650-E657.

With adequ. protein and nutrients "crash"- beats "low and steady" -dieting. In the obese that's almost certain, in athletes more experimental evidence are needed.

You will have heard and read that rapid weight loss will make you lose muscle and set you up for weight regain aka the "Yo-Yo effect". As a waredownloadsoft reader, you know that things are not as simple as that. While some studies appear to support this urban myth others suggest that the exact opposite may be the case.

A 2014 study by Purcell, Sumithran, and Prendergast that was published in the venerable scientific journal The Lancet for example, showed that rapid weight loss on a very low calorie diet leads to better long-term outcomes than gradual weight loss on a much less restricted diet.
That's a results of which I feel that it is important enough to re-address ii in its own waredownloadsoft article. After all, the "slow and steady" advise is still ubiquitous, both in the mainstream and in the health and fitness community. In said study, Purcell et al.

"aimed to investigate whether the rate of weight loss affects the rate of regain, and whether weight lossinduced changes in circulating appetite-mediating hormones and subjective appetite are affected by the rate of weight loss" (Purcell. 2012).

To this end, the researchers from the University of Melbourne conducted a two-phase, non-masked, randomized controlled trial. The study participants were recruited through radio and newspaper advertisements and word of mouth in Melbourne, Australia.

• Inclusion criteria were healthy men and women aged between 18–70 years who were weight stable for 3 months and had a BMI between 30.0–45.0kg/m². 
• Exclusion criteria included use of a very low energy diet or weight loss drugs in the previous 3 months, contraceptive use, pregnancy or lactation, smoking, current use of drugs known to affect body weight, previous weight loss surgery, and the presence of clinically significant disease (including diabetes).

Eligible participants were randomized into 2 different weight loss programs — a 12-week rapid program or a 36-week gradual program —using a computer-generated randomization sequence with a block design to account for the potential confounding factors of age, sex, and body mass index (BMI). Investigators and laboratory staff were blind to the group assignments.

Figure 1: Overview of the study design (Purcell. 2014)

Both, the subjects on the rapid and the gradual weight loss program had the same simple goal: "Reduce your body weight by at least 12.5%." The way the subjects were supposed to achieve this weight loss was yet completely different. For phase 1 of the study (until 12.5% weight loss), the following interventions were prescribed:

• Better ZERO than Some Food? Study Suggest Just That! Learn more.

  Rapid weight loss: Participants in the rapid weight loss group replaced 3 meals a day with a commercially available meal replacement (Optifast, Nestlé Nutrition) over a period of 12 weeks (450–800 kcal/day). 
• Gradual weight loss: Participants in the gradual group replaced 1 to 2 meals daily with the same supplements and followed a diet program based on recommendations from the Australian Guide to Healthy Eating for the other meals over a period of 36 weeks (400–500 kcal deficit per day).

Both groups were given comparable dietary education materials and had appointments every 2 weeks with the same dietician. Participants who achieved 12.5% or greater weight loss were eligible for phase 2. In phase 2, participants met with their same dietician at weeks 4 and 12, and then every 12 weeks until week 144. During appointments, the dietician assessed adherence based on participants' self-reported food intake, and participants were encouraged to partake in 30 minutes of physical activity of mild to moderate intensity. Participants who gained weight were told to reduce their energy intake by 400–500 kcal in order to get back on the weight loss track.
To assess the success of the diets, the scientists used the mean weight loss that was maintained at week 144 of phase 2 (primary outcome), the mean difference in fasting ghrelin and leptin concentrations measured at baseline, end of phase 1 (week 12 for rapid and week 36 for gradual), and at weeks 48 and 144 of phase 2, as well as the overall changes in weight, BMI, waist and hip circumferences, fat mass, fat free mass, ghrelin, leptin, and physical activity (secondary outcomes).

Figure 2: Percent of participants achieving the weight loss target in phase 1 completers (left) and all subjects including the losers who didn't complete the full study - that the right figure shows even greater differences actually supports the superiority of the rapid vs. gradual weight loss regimen (p = 0.0001 | Purcell. 2015)

The overall message of the results was clear, the "rate of weight loss does not affect the proportion of weight regained within 144 weeks" (Purcell. 2014). The same goes for the implication that "[t]hese findings are not consistent with present dietary guidelines which recommend gradual over rapid weight loss, based on the belief that rapid weight loss is more quickly regained" (ibid).

Figure 3: Relative changes in measures body composition (left) and activity from pre- to follow up (Purcell. 2015).

But this wouldn't be the waredownloadsoft if we didn't go beyond the mere averages for the main study outcomes. So, let's take a look at the actual changes from the pretest to the follow up in Figure 3. What do you see? Yes, the rapid weight loss group had better (albeit not significantly better) results in everything and that despite the fact that they didn't increase their physical activity (see Figure 2, right). So let's not forget that this information that's missing from the abstract, when we're discussing the "bottom line" to this article in the following paragraphs.
References:

• Bistrian, B. R., and Mindy Sherman. "Results of the treatment of obesity with a protein-sparing modified fast." International journal of obesity 2.2 (1977): 143-148.
• Garthe, Ina, et al. "Effect of two different weight-loss rates on body composition and strength and power-related performance in elite athletes." International journal of sport nutrition and exercise metabolism 21 (2011): 97-104.
• Iselin, Hans U., and Peter Burckhardt. "Balanced hypocaloric diet versus protein-sparing modified fast in the treatment of obesity: a comparative study." International journal of obesity (1982).
• Martin, Corby K., et al. "Empirical evaluation of the ability to learn a calorie counting system and estimate portion size and food intake." British Journal of Nutrition 98.2 (2007): 439-444.
• Martin, Corby K., and Kishore M. Gadde. "Weight loss: slow and steady does not win the race." The Lancet Diabetes & Endocrinology 2.12 (2014): 927-928.
• Mero, Antti A., et al. "Moderate energy restriction with high protein diet results in healthier outcome in women." J Int Soc Sports Nutr 7.4 (2010): 1-11.
• Nackers, Lisa M., Kathryn M. Ross, and Michael G. Perri. "The association between rate of initial weight loss and long-term success in obesity treatment: does slow and steady win the race?." International journal of behavioral medicine 17.3 (2010): 161-167.
• Purcell, Katrina, et al. "The effect of rate of weight loss on long-term weight management: a randomised controlled trial." The Lancet Diabetes & Endocrinology 2.12 (2014): 954-962.
• Rolls, Barbara J., P. M. Van Duijvenvoorde, and Edmund T. Rolls. "Pleasantness changes and food intake in a varied four-course meal." Appetite 5.4 (1984): 337-348.

You don't need supplemental K, well... unless you are on a protein modified fast without fruits and veggies ;-)

The 1984 study by Norbiato et al. is not a very recent, but it's probably a very important study which was set up to investigate "the role of potassium deficiency in the development of glucose intolerance during caloric deprivation" (Norbiato. 1984).

Or, put simly, the scientists wanted to know if a low potassium level may promote insulin resistance and modify or is modified in response to dieting (in this case protein-modified fasting). In the study, two groups of subjects were studied. The "normal" group consisted of ten subjects, who were 27-45 years old and whose body weights ranged from 89 to 115% of the "ideal body weight". The "obese" group group consisted of twenty subjects aged 21-48 years who were 70%-131% overweight.
Before the obese subjects were put on a protein modified fast (PMF) all subjects, lean or obese, received a "weight-maintaining diet" with 200g/day carbohydrates for 8 days.

Figure 1: Macronutrient composition of the ~380kcal PMF diet (Norbiato. 1984).

"The diets were calculated according to individual tastes, employing varying proportions of egg white, beef tenderloin, skim-milk cheese and water-packed canned tuna. For the PMF, total calories varied from a mean of 350-399 in individual subjects, with a mean of 378+/-36 (SD) 

[...] Calculated protein intakes, according to standard tables, were 70.8+/-7.6 g/day (about 79% of calories). Calculated fat intake was 5.7+/-3.5 g /day (19% of calories). Carbohydrate contributed 3.2+/-1.3 g/day, 2% of caloric input" (Norbiato. 1984).

As far as its potassium content is concerned the PMF diet was (as probably most diets that are almost exclusively protein) on the skinny side (15 +/- 3.9 mmol of potassium/day | adult men and women should get 100mmol/day and 72mmol/day, that's 3,800mg and 2,800mg/day or 8-9 bananas if you want to "go bananas" instead of leafy greens ;-). Nevertheless, only 10 out of 20 of the obese subjects received an oral potassium chloride (64 mmol/day) supplement (KC1-retard, Zyma, Italy). The other ten patients received identical placebo tablets.
Interestingly, the potassium levels dropped in both groups during fasting. More importantly, though, the decrease in potassium was associated with a sign. reduction in peripheral levels of insulin along with an increase in insulin receptors and a striking reduction of peripheral glucose utilization in the obese subjects on their protein modified fast.

Figure 2: Mean integrated area under the glucose tolerance test curve in obese subjects submitted to protein-modified fast (PMF) with or without oral KCl supplementation (K): studies were performed in the control period after a 14-day fast and after after 10 days of refeeding with a diet containing 700 kcal (45% carbohydrate) per day (Norbiato. 1984).

Increase in insulin receptor binding and impaired glucose management? How does this go together? Well, if the receptor does not respond, it is no wonder that the researchers found that their subjects ability to handle glucose was significantly impaired in the euglycaemic clamp study.
References:

• Norbiato, Guido, et al. "Effects of potassium supplementation on insulin binding and insulin action in human obesity: protein‐modified fast and refeeding." European journal of clinical investigation 14.6 (1984): 414-419.
• Rowe, John W., et al. "Effect of experimental potassium deficiency on glucose and insulin metabolism." Metabolism 29.6 (1980): 498-502.

It were the nightly binges, not the fasting that made the rodents fat... and it's not news that starving and bingeing is obesogenic, is it?

Recently, Kara L. Kliewer and her colleagues, probably tried to do something good, when they conducted a study to "capture intraday oscillations in lipid stores and adipose tissue gene expression in gorging mice and to identify metabolic consequences of gorging precipitated by food restriction during weight regain" (Kliewer. 2015). Whether what came out of it, i.e. articles saying that "Skipping Meals Promotes Belly Fat Storage, Increases Risk For Insulin Resistance" (MedicalDaily), however, will help people avoid help you lose body or belly fat appears to be highly questionable, though. After all, the mainstream interpretation of the study is rigid with respect to its implications.
Before we delve further into the details, however, let's briefly take a look at what the researchers from the Ohio State University actually did: As you can see in Figure 1 we are - and this is by no means clear whence you're reading only the press-release "copy-and-paste"-jobs online - actually dealing with a feeding regimen that looks pretty similar to what people usually think of when they are talking about intermittent fasting.

Figure 1: Feeding and fasting cycles and metabolic states in 24h feeding cycle (Kliewer. 2015).

So, basically, we are talking about a ~15h fast with that is followed by a 7h feeding window. But there are significant differences to intermittent fasting in humans:

1. Gorging is not allowed on IF-regimen - Usually people who follow intermittent fasting regimens are somewhat anal about their nutrition. A binge like the one that occurred in the mice during the feeding phase is therefore representative mostly of the obese who don't "fast" in the sense of "intermittent fasting", but try to starve themselves for 24h failing only to fall victim to their own cravings late at night (remember: mice are active at night, so their biological clock is inverted compare to ours).
2. Feeding does not occur at the wrong time on IF-regimen - Since we are already talking about "falling victim to [one's] cravings late at night," someone doing a real IF-regimen would never feed at night. He would do it in the early to late afternoon to avoid messing with his cicrcadian rhythm. The mice in the study at hand, however, were fat one-third into the "light period", which is their night and according to the rodents' biological clock not a proper time to "gorge".

Against that background I would be more than hesitant to use the study at hand as evidence of the adipogenic effects of intermittent fasting.

Figure 2: Yes, there's an increase in body weight (albeit not to the same weight as in the control group) and there is an increase in body fat, but both are due to "binging" not due to fasting (Kliewer. 2015).

Rather than that, you will probably see increases in visceral body fat as they are shown in Figure 2 (right hand side) in the previously mentioned "failed self-starvers" who starve all-day and gorge at night - none of my previous intermittent fasting suggestions involved either of these practices (i.e. starving and gorging).
I am thus pretty sure that you have not ruined your body composition if you've been skipping breakfast or even breakfast and launch recently; and that's even more true, if you have followed my advice to use intermittent fasting as a short-term program to lose fat by combining timing and energetic restriction to your advantage.

If you have don just that, you don't have to care about the idiots who are still trying to propagate the myth of "frequent meals for fat loss". If they (a) knew the difference between intermittent fasting and starving and (b) had not relied on an already messed up press release, but had read the study, they would have been aware that  the researchers themselves state that the mechanism for the increased fat gains still has to be elucidated:

"Future studies should determine whether changes in adipose tissue gene expressions, lipid stores, and whole-body metabolism in our study can be attributed to the initial food restriction, circadian disturbances, and/or gorging eating pattern" (Kliewer. 2015).

And let's be honest, do you really think it's the meal skipping, not gorging at a (internal clock-wise) totally wrong time that made the mice fat? If so, you have probably been exposed to too much "frequent meal propaganda" in the past years.
References:

• Kliewer, Kara L., et al. "Short-term food restriction followed by controlled refeeding promotes gorging behavior, enhances fat deposition, and diminishes insulin sensitivity in mice." The Journal of nutritional biochemistry (2015).